Search

Introduction Although depression is often associated with poor glycemic control in patients with type 2 diabetes mellitus (T2DM), this observation has been inconsistent. This exploratory, post hoc analysis investigated associations between depression parameters and glycemic control using data from a 24-month, prospective, observational, non-interventional study evaluating glycemic response following insulin initiation for T2DM. Methods We analyzed data from a 24-month, prospective, observational study that evaluated glycemic response in patients with T2DM who initiated insulin therapy (N = 985) in 5 European countries. Secondary measures included patient-reported diagnosis of depression at baseline, severity of depressed/anxious mood (EuroQol (EQ)-5D item) and diabetes-related distress (Psychological Distress domain of the Diabetes Health Profile, DHP-18). The latter two measures were assessed at baseline and 5 time points throughout the study. Glycemic control was measured by glycated hemoglobin (HbA1c) at these same time points. Analyses employed t tests to assess the unadjusted baseline difference in HbA1c between patients with and without the respective depression parameter. The potential effect of demographic and clinical confounding variables was controlled through a linear model structure. Patient HbA1c levels were analyzed by presence/absence of a history of diagnosed depression, depressed mood, and diabetes-related distress. Results Patients with higher depression parameters or distress at baseline had significantly higher rates of microvascular complications at baseline. Patients with a history of diagnosed depression or high diabetes-related distress had higher HbA1c than patients without. HbA1c of patients with or without depressed mood was not significantly different at baseline. The proportion of patients with depressed mood declined after insulin initiation, whereas the proportion of patients with high diabetes-related distress did not significantly change. HbA1c improved following insulin initiation, regardless of presence/absence of studied depression/distress parameters at baseline. Conclusion History of diagnosed depression, diabetes-related distress, and depressed mood were associated with a higher rate of microvascular complications. Diagnosed depression and diabetes-related distress also showed higher HbA1c at baseline when insulin was initiated. Insulin therapy improved glycemic control, while preexisting depressed mood declined and diabetes-related distress remained unchanged. Electronic supplementary material The online version of this article (doi:10.1007/s13300-015-0118-y) contains supplementary material, which is available to authorized users.

Purpose Although diabetes is recognized as a risk factor for the development of cognitive impairment and for accelerated progression to Alzheimer disease (AD), it is unclear whether patients with diabetes who have already progressed to AD have a different rate of cognitive and functional decline compared with that in those without diabetes. This post hoc exploratory analysis compared cognitive and functional decline over an 18-month period in patients with mild AD dementia with and without comorbid diabetes. Decline in quality of life was assessed as a secondary objective. Methods In a post hoc exploratory analysis, we analyzed data from the placebo groups of three 18-month, randomized, placebo-controlled trials of solanezumab and semagacestat in patients with AD. Data from patients with mild AD dementia (Mini-Mental State Examination [MMSE] score, 20–26) and comorbid diabetes at baseline were compared with data from patients with mild AD dementia without diabetes at baseline. Cognition was assessed using the 14-item AD Assessment Scale–Cognitive Subscale (ADAS-Cog 14 ) and the MMSE. Functioning was assessed with the AD Cooperative Study–Activities of Daily Living Inventory (instrumental subset) (ADCS-iADL). Quality of life was assessed using the European Quality of Life–5 Dimensions scale, proxy version (proxy utility score and visual analog scale score), and the Quality of Life in AD scale, self-report and proxy (caregiver) versions. Group comparisons of changes from baseline to 18 months in cognitive, functional, and quality-of-life measures employed a repeated-measures model adjusted for propensity score, study, baseline cognition score (functional or quality of life), age, sex, level of education, genotype of the apolipoprotein E gene, and concurrent use of an acetylcholinesterase inhibitor or memantine. Findings At baseline, patients with mild AD dementia with and without diabetes did not significantly differ on the cognitive measures, but those without diabetes were functioning at a significantly higher level. At 18 months, compared with patients without diabetes, those with diabetes showed a numerically but statistically nonsignificantly lesser cognitive decline (least squares mean between-group differences: ADAS-Cog 14 score, 1.61 [ P = 0.21]; MMSE score, –0.40 [ P = 0.49]) and a statistically significantly lesser functional decline (least squares mean between-group difference in ADCS-iADL score, –3.07; P = 0.01). The 2 groups did not differ on declines in the quality-of-life measures. Implications The present findings suggest that diabetes may influence the rate of functional decline among patients with mild AD dementia. These results require replication in studies that address the limitations of the present post hoc exploratory analysis and that explore the potential causes of the observed differences.

The American Diabetes Association consensus statement on the treatment of type 2 diabetes mellitus (T2DM) in older patients highlights the need for treatment pattern and effectiveness data from real-world settings and populations. This retrospective cohort study assessed the relative frequency of use of four commonly prescribed antihyperglycemia treatments for T2DM and quantified their effectiveness up to 2 years post-initiation.Within a large, U.S.-based, electronic health record database, we investigated usage of insulin, sulfonylureas, glucagon-like peptide-1(GLP-1) receptor agonists, and dipeptidyl peptidase-4 (DPP-4) inhibitors in patients with T2DM, focusing on those ≥65 years old, although younger patients were included for comparative purposes.Inclusion criteria were met by 77,440 patients. Mean baseline glycosylated hemoglobin (HbA1c) levels for patients ≥65 years old varied among treatments: insulin (7.7% [61 mmol/mol]; n=3,311), sulfonylureas (7.0% [53 mmol/mol]; n=5,706), GLP-1 receptor agonists (7.1% [54 mmol/mol]; n=260), and DPP-4 inhibitors (7.1% [54 mmol/mol]; n=1,096). Older patients demonstrated good glycemic control at therapy initiation and were prescribed glucose-lowering agents at lower HbA1c values compared with younger patients. A large proportion of older patients were prescribed sulfonylureas (56%) and insulin (34%) compared with GLP-1 receptor agonists (3.4%) and DPP-4 inhibitors (12%), despite the associated risk of hypoglycemia.Patients initiating insulin and sulfonylureas demonstrated more sustained glycemic control compared with GLP-1 receptor agonists and DPP-4 inhibitors. A majority of older patients with T2DM was initiated on sulfonylureas and insulin at relatively low levels of HbA1c, a practice not entirely consistent with the recommendations of published guidelines.

The objective of this study was to apply quantile regression (QR) methodology to a population from a large representative health insurance plan with known skewed healthcare utilization attributes, co-morbidities, and costs in order to identify predictors of increased healthcare costs. Further, this study provides comparison of the results to those obtained using ordinary least squares (OLS) regression methodology.Members diagnosed with Type 2 Diabetes and with 24 months of continuous enrollment were included. Baseline patient demographic, clinical, consumer/behavioural, and cost characteristics were quantified. Quantile regression was used to model the relationship between the baseline characteristics and total healthcare costs during the follow-up 12 month period.The sample included 83,705 patients (mean age = 70.6 years, 48% male) residing primarily in the southern US (78.1%); 81.2% of subjects were on oral-only anti-diabetic therapy. Co-morbid conditions included nephropathy (43.5%), peripheral artery disease (26.4%), and retinopathy (18.0%). Variables with the strongest relationship with costs during the follow-up period included outpatient visits, ER visits, inpatient visits, and Diabetes Complications Severity Index score during the baseline period. In the top cost quantiles, each additional glycohemoglobin (HbA1c) test was associated with cost savings ($1400 in the 98th percentile). Stage 4 and Stage 5 chronic kidney disease were associated with an incremental cost increase of $33,131 and $106,975 relative to Stage 1 or no CKD in the 98th percentile ($US).These results demonstrate that QR provides additional insight compared to traditional OLS regression modeling, and may be more useful for informing resource allocation to patients most likely to benefit from interventions. This study highlights that the impact of clinical and demographic characteristics on the economic burden of the disease vary across the continuum of healthcare costs. Understanding factors that drive costs on an individual patient level provide important insights that will help in ameliorating the clinical, humanistic, and economic burden of diabetes.

Laparoscopic Roux-en-Y gastric bypass (LRYGB) achieves sustainable weight loss possibly by altering the gut microbiota. The effect of a proton pump inhibitor (PPI) on weight loss and the gut microbiota has not been explored. PPI use and the gut microbiota were assessed before and 6 months after LRYGB in eight patients. Bacterial profiles were generated by 16S ribosomal RNA (rRNA) gene sequencing. Prior to LRYGB, PPI users had a higher percent relative abundance (PRA) of Firmicutes compared to nonusers. PPI users at 6 months post-LRYGB had a higher PRA of Firmicutes [48.6 versus 35.6 %, p = nonsignificant (NS)] and a trend toward significantly lower percent excess weight loss (49.3 versus 61.4 %, p = 0.067) compared to nonusers. PPI use post-LRYGB may impair weight loss by modifying gut microbiota.

Baseline cardiovascular characteristics and longitudinal changes following weight loss surgery (WLS) in adolescents are not well defined. Recent data suggest that the use of transthoracic echocardiography (TTE) for preoperative cardiac assessment may provide suboptimal imaging fidelity secondary to excessive upper body adiposity. High fidelity imaging using cardiac magnetic resonance (CMR) is an extremely useful diagnostic tool. We report the use of CMR in a cohort of extremely obese adolescents undergoing WLS.A retrospective analysis of adolescent WLS patients at a single institution was conducted. Data collection included mean age, sex, body mass index (BMI), and CMR measurements of left ventricular (LV) mass, LV end-diastolic volume (LVEDV), ejection fraction (EF), and myocardial perfusion reserve index (MPRI). Comparison of CMR results to normative data derived from lean subjects was performed.Ten subjects (9 female), with a mean age and BMI of 17.4 ± 1.9 years and 50.33 ± 10.21 kg/m(2) respectively, were studied. When compared to age, gender, and height matched normal weight (NW) controls, the obese (OB) subjects had evidence of increased LV mass (122 ± 25 g vs. 101 ± 10 g, OB vs. NW respectively, p0.05), and increased LVEDV (156 ± 25 mL vs. 109 ± 9 mL, p0.05), with an average EF of 61.5% ± 5% (range 52% to 67% vs. 71% to 74% expected EF for males and females, respectively, p=0.003). In addition, 60% of the OB subjects (6/10) demonstrated adenosine-induced sub-endocardial ischemia at baseline, the majority of whom underwent WLS (n=5) resulting in complete normalization of ischemia in 60% (3/5) and partial improvement in 40% (2/5). A reduction in mean LV mass (range 2 to 12 g) following WLS was observed.Extreme adolescent obesity is associated with significant cardiovascular abnormalities that include LV hypertrophy (i.e. increased LV mass) and LV dilatation. These findings, considered to be well-recognized cardiovascular disease risk factors in adults, were shown to be reversible after WLS in the small group of subjects studied here. Additional large-scale investigations designed to examine obesity-related cardiovascular disease in severely obese adolescents are required.

Background The burden on caregivers of patients with Alzheimer’s disease (AD) is associated with the patient’s functional status and may also be influenced by chronic comorbid medical conditions, such as diabetes. This post-hoc exploratory analysis assessed whether comorbid diabetes in patients with AD affects caregiver burden, and whether caregivers with diabetes experience greater burden than caregivers without diabetes. Caregiver and patient healthcare resource use (HCRU) were also assessed. Methods Baseline data from the GERAS observational study of patients with AD and their caregivers (both n = 1495) in France, Germany and the UK were analyzed. Caregiver burden was assessed using the Zarit Burden Interview (ZBI). Caregiver time on activities of daily living (ADL: basic ADL; instrumental ADL, iADL) and supervision (hours/month), and caregiver and patient HCRU (outpatient visits, emergency room visits, nights hospitalized) were assessed using the Resource Utilization in Dementia instrument for the month before the baseline visit. Regression analyses were adjusted for relevant covariates. Time on supervision and basic ADL was analyzed using zero-inflated negative binomial regression. Results Caregivers of patients with diabetes (n = 188) were younger and more likely to be female (both p

Despite evidence for higher fracture risk, clinical effects of osteoporosis treatments in type 2 diabetes (T2D) are largely unknown. Post hoc analyses of the DANCE observational study compared T2D patients and patients without diabetes to assess the effect of teriparatide, an osteoanabolic therapy on skeletal outcomes and safety. Patients included ambulatory men and women with osteoporosis receiving teriparatide 20μg/day SQ up to 24months followed by observation up to 24months. Main outcome measures included nonvertebral fracture incidence comparing 0-6months with 6+ months of teriparatide, change from baseline in BMD and back pain severity, and serious adverse events. Analyses included 4042 patients; 291 with T2D, 3751 without diabetes. Treatment exposure did not differ by group. For T2D patients, fracture incidence was 3.5 per 100 patient-years during 0-6months treatment, and 1.6 during 6months to treatment end (47% of baseline, 95% CI 12-187%); during similar periods, for patients without diabetes, fracture incidence was 3.2 and 1.8 (57% of baseline, 95% CI 39-83%). As determinants of fracture outcome during teriparatide treatment, diabetes was not a significant factor (P=0.858), treatment duration was significant (P=0.003), and the effect of duration was not significantly different between the groups (interaction P=0.792). Increases in spine and total hip BMD did not differ between groups; increase in femoral neck BMD was greater in T2D patients than in patients without diabetes (+0.34 and +0.004g/cm(2), respectively; P=0.014). Back pain severity decreased in both groups. Teriparatide was well tolerated without new safety findings. In conclusion, during teriparatide treatment, reduction in nonvertebral fracture incidence, increase in BMD, and decrease in back pain were similar in T2D and non-diabetic patients.

Supplementation of standardized fermented papaya preparation (FPP) to adult diabetic mice improves dermal wound healing outcomes. Peripheral blood mononuclear cells (PBMC) from type II diabetes mellitus (T2DM) patients elicit a compromised respiratory burst activity resulting in increased risk of infections for the diabetic patients. Aims: The objectives of the current study were to determine the effect of FPP supplementation on human diabetic PBMC respiratory burst activity and to understand underlying mechanisms of such action of FPP. Results: When stimulated with phorbol 12-myristate 13-acetate, the production of reactive oxygen species by T2DM PBMC was markedly compromised compared to that of the PBMC from non-DM donors. FPP treated ex vivo improved respiratory burst outcomes in T2DM PBMC. FPP treatment significantly increased phosphorylation of the p47phox subunit of NADPH oxidase. In addition, the protein and mRNA expression of Rac2 was potently upregulated after FPP supplemention. The proximal human Rac2 gene promoter is G–C rich and contains consensus binding sites for Sp1 and AP-1. While FPP had no significant effect on the AP-1 DNA binding activity, the Sp1 DNA binding activity was significantly upregulated in PBMC after treatment of the cells with FPP. Innovation: This work provided first evidence that compromised respiratory burst performance of T2DM PBMC may be corrected by a nutritional supplement. Conclusion: FPP can correct respiratory burst performance of T2DM PBMC via an Sp-1-dependant pathway. Studies testing the outcome of FPP supplementation in diabetic patients are warranted. Antioxid. Redox Signal. 17, 485–491.

Aim: To determine whether an insulin algorithm could be used in a similar manner in the setting of diabetes and stress hyperglycaemia following cessation of intravenous (IV) insulin after cardiac surgery. Methods: Subjects who were clinically stable, requiring ≥1 unit/h of IV insulin 48 h after surgery, were randomized to once daily detemir at 50, 65 or 80% of IV insulin requirements and received aspart according to carbohydrate intake. Diabetes was defined as any history of diabetes or preoperative HbA1c 6.5%. Results: The morning glucose in patients with diabetes was 143 mg/dl (n = 61) vs. 124 mg/dl in those with stress hyperglycaemia (n = 21,p = 0.05) on day 1 and 127 vs. 110 mg/dl over 72 h (p = 0.01). This was unaffected by adjustment for initial dosing group. At 72 h, 56% of patients with stress hyperglycaemia reached AM (80–130 mg/dl) and 87% reached overall (80–180 mg/dl) glucose targets, compared to 90 and 100% of patients with stress hyperglycaemia, respectively. There was no difference in hypoglycaemia in patients with stress hyperglycaemia or diabetes. The percentage of patients with diabetes receiving insulin was 46% on admission and 77% at discharge, compared to 0 and 42% of patients with stress hyperglycaemia. Conclusions: Following cardiac surgery, patients with stress hyperglycaemia may be converted from IV insulin to detemir with a 50% conversion factor, while patients with diabetes may require a higher conversion factor. Stress hyperglycaemia may be prolonged; the intensity and duration of insulin therapy required for optimal outcomes warrants further examination.

Bariatric surgery results in durable weight loss and improved comorbidities. The objectives of this study were to examine the efficacy of gastric bypass in reducing comorbid burden and improving metabolic status among morbidly obese adolescents. The medical records of 15 gastric bypass patients were retrospectively reviewed. Changes in metabolic markers were determined at baseline, 1 and 2 years post-operatively. Comparative analysis demonstrated significant improvement in weight, BMI, insulin, HbA1C, C-peptide, %B, %S, IR, cholesterol, percentile cholesterol, TG, percentile TG, HDL, percentile HDL, LDL, percentile LDL, and VLDL. Results support bariatric surgery as a treatment for morbidly obese adolescents with comorbidities.

Background : Glycemic control is an important aspect of patient care in the surgical intensive care unit (SICU). This is a pilot study of a novel glycemic analysis tool - the glucogram. We hypothesize that the glucogram may be helpful in quantifying the clinical significance of acute hyperglycemic states (AHS) and in describing glycemic variability (GV) in critically ill patients. Materials and Methods: Serial glucose measurements were analyzed in SICU patients with lengths of stay (LOS) >30 days. Glucose data were formatted into 12-hour epochs and graphically analyzed using stochastic and momentum indicators. Recorded clinical events were classified as major or minor (control). Examples of major events include cardiogenic shock, acute respiratory failure, major hemorrhage, infection/sepsis, etc. Examples of minor (control) events include non-emergent bedside procedures, blood transfusion given to a hemodynamically stable patient, etc. Positive/negative indicator status was then correlated with AHS and associated clinical events. The conjunction of positive indicator/major clinical event or negative indicator/minor clinical event was defined as clinical match. GV was determined by averaging glucose fluctuations (maximal - minimal value within each 12-hour epoch) over time. In addition, event-specific glucose excursion (ESGE) associated with each positive indicator/AHS match (final minus initial value for each occurrence) was calculated. Descriptive statistics, sensitivity/specificity determination, and student's t-test were used in data analysis. Results : Glycemic and clinical data were reviewed for 11 patients (mean SICU LOS 74.5 days; 7 men/4 women; mean age 54.9 years; APACHE II of 17.7 ± 6.44; mortality 36%). A total of 4354 glucose data points (1254 epochs) were analyzed. There were 354 major clinical events and 93 minor (control) events. The glucogram identified AHS/indicator/clinical event matches with overall sensitivity of 84% and specificity of 65%. We noted that while the mean GV was greater for non-survivors than for survivors (19.3 mg/dL vs. 10.3 mg/dL, P = 0.02), there was no difference in mean ESGE between survivors (154.7) and non-survivors (160.8, P = 0.67). Conclusions: The glucogram was able to quantify the correlation between AHS and major clinical events with a sensitivity of 84% and a specificity of 65%. In addition, mean GV was nearly two times higher for non-survivors. The glucogram may be useful both clinically (i.e., in the electronic ICU or other early warning systems) and as a research tool (i.e., in model development and standardization). Results of this study provide a foundation for further, larger-scale, multi-parametric, prospective evaluations of the glucogram.

Background Diabetes and CHF are common comorbidities in hospitalized patients but the relationship between glycaemic control, glycaemic variability, and mortality in patients with both conditions is unclear. Methods We used administrative data to retrospectively identify patients with a diagnosis of CHF who underwent frequent glucose assessments. TWMG was compared with other measures of glycaemic control and a time-weighted measure of glycaemic variability, the glycaemic lability index. The outcome was hospital mortality. Results A total of 748 patients were included in the final analysis. Time-weighted mean glucose was higher than unadjusted mean glucose (137 + /− 44.7 mg/dL versus 167 + /− 54.9, p < 0.001), due in part to shorter sampling intervals at higher glucose levels. Hypoglycaemia, defined as a glucose level < 70 mg/dL, occurred during 6.3% of patient-days in survivors and 8.4% of patient-days among nonsurvivors (p = 0.05). Time-weighted mean glucose was similar (128 + /− 33.1 mg/dL versus 138 + /− 45.1 mg/dL) in nonsurvivors versus survivors, p = 0.19). However, relatively few patients had were significantly elevated readings. Median GLI was higher in nonsurvivors compared with that in survivors (18.1 versus 6.82, p = 0.0003). Increasing glycaemic lability index (odds ratio 1.32, 95% confidence interval 1.05–1.65), and hypoglycaemia (odds ratio 2.21, 95% confidence interval 1.07–4.65), were independently associated with higher mortality in logistic regression analysis. Respiratory failure was associated with mortality, but not standard deviation of glucose. Conclusions Future studies analysing glycaemic control should control for variable sampling intervals. In this analysis, glycaemic lability index was independently associated with increased mortality, independent of hypoglycaemia. Prospective studies are needed to evaluate these findings. Copyright © 2010 John Wiley & Sons, Ltd.

To determine the relationship between inpatient glycemic control and hospital readmission in patients with congestive heart failure (CHF).We used an electronic data collection tool to identify patients with a discharge diagnosis of CHF who underwent point-of-care glucose assessments. Timeweighted mean glucose (TWMG), hemoglobin A1c, and glycemic lability index (GLI) served as glycemic indicators, and readmission for CHF was determined at 30 days and between 30 and 90 days.The analysis included 748 patients. After adjustment for significant covariates, log-transformed increasing TWMG (odds ratio 3.3; P = .03) and log-transformed hemoglobin A1c (odds ratio 5.5; P = .04) were independently associated with higher readmission for CHF between 30 and 90 days, but not by 30 days. Renal disease, African American race, and year of hospital admission were also significantly associated with readmission, but GLI was not. There was no significant difference in TWMG when analyzed on the basis of race or renal status. We noted a decrease in TWMG (P = .004) and a trend for reduction in readmission rates between 30 and 90 days (P = .06) after hospital-wide interventions were implemented to improve glycemic control, but no significant difference was detected in GLI or hypoglycemia.Increasing glucose exposure, but not glycemic variability, was associated with higher risk of readmission between 30 and 90 days in patients with CHF. Prospective studies are needed to confirm or refute these results.

Metabolic syndrome (MetS) as defined by the Adult Treatment Panel (ATP) III criteria includes 3 metabolic parameters: serum glucose, triglycerides, and high-density lipoprotein cholesterol (HDL-C) measurements. However, the impact of each of the 3 metabolic parameters on cardiovascular disease (CVD) risk in African American women (AAW) is unknown. Therefore, we investigated CVD risk clusters associated with each of the 3 metabolic components of MetS in adult nondiabetic, overweight/obese AAW. We studied the clinical and metabolic CVD risk factors of 258 AAW (mean age, 42.4 +/- 8.4 years; mean body mass index, 33.4 +/- 8.0 (kg/m(2)). Fasting serum insulin, glucose, and C-peptide levels were obtained in each subject. Waist circumference and systolic and diastolic blood pressure were measured. Insulin sensitivity (Bergman minimal model method) and insulin resistance (homeostasis model assessment) were calculated. We examined the prevalence of MetS and its components associated with each of the 3 metabolic components (ie, serum glucose, HDL-C, and triglycerides) of the MetS as defined by ATP III. Worsening of any of the 3 metabolic parameters was associated with increasing waist circumference but not with age and body mass index nor with insulin, C-peptide, homeostasis model assessment of insulin resistance, and insulin sensitivity. As a group, the prevalence of MetS was 35.5% in our AAW. The prevalence of MetS increased 3-fold from first to third tertiles of serum glucose (14.1% and 42.3%, respectively). Worsening of serum HDL-C from tertiles 3 to 1 was associated with significant increases in the prevalence of MetS (1.2% vs 42.3%, respectively). Comparing first with third tertile of triglycerides, there was no significant increase in MetS in our AAW (7% vs 17%). Contrasting the 3 metabolic components, the prevalence of MetS was higher in the third tertile of glucose (43.2%) and first tertile of HDL-C (42.3%) and least with the third tertile of triglycerides (17%). In summary, each of the metabolic components of MetS was associated with different degrees of the clustering of CVD risk factors in AAW. We found that alterations in serum glucose and HDL-C were more predictive of MetS, each yielding approximately 40% of the prevalence of MetS in our nondiabetic, obese AAW. We found that triglycerides had the least impact on MetS in our AAW. We propose (1) that the 3 metabolic parameters for MetS defined by ATP III should be weighted differently with respect to their potential for CVD risks and perhaps outcomes and (2) that nondiabetic AAW in our third tertile of serum glucose (100 mg/dL) and/or first tertile of HDL-C (40 mg/dL) should be targeted for screening for MetS.

Aims To assess the awareness of risk factors for type 2 diabetes and lifestyle changes that can decrease such risks in women with GDM. Methods The study comprised responses to health questionnaires by 319 women: 31 pregnant women with current GDM (CGDM), 88 women with previous GDM (PGDM), 100 pregnant women without DM (PWDM) and 100 non-pregnant women without DM (NPWDM). The CGDM group answered the questionnaires at the initiation and 4 weeks after participating in formal education on GDM. Two types of awareness scores (AS) were established. One AS was about the risks associated with GDM (GDMR), and the other was related to the awareness of lifestyle changes that can decrease the risks of type 2 diabetes (DM2R). Results The PGDM group had the highest GDMR and DM2R scores (9.55 ± 2.66) (13.2 ± 2.26) compared with the other groups (CGDM 7.48 ± 3.14, NPWDM 6.10 ± 3.17, PWDM 2.89 ± 2.48) ( p p p p Conclusions Women had limited awareness of risk factors for type 2 diabetes and lifestyle modifications that can decrease such risk of diabetes. AS were higher in women with current and previous GDM after receiving formal education.

Short-term aerobic exercise training can improve whole-body insulin sensitivity in humans with type 2 diabetes mellitus; however, the contributions of peripheral and hepatic tissues to these improvements are not known.Our objective was to determine the effect of 7-d aerobic exercise training on peripheral and hepatic insulin sensitivity during isoglycemic/hyperinsulinemic clamp conditions.Subjects were randomly assigned to one of two groups. The energy balance group consumed an isocaloric diet consisting of 50% carbohydrate, 30% fat, and 20% protein for 15 d. The energy balance plus exercise group consumed a similar diet over the 15 d and performed 50-min of treadmill walking at 70% of maximum oxygen consumption maximum during the second 7 d of the 15-d study period. Each subject underwent an initial isoglycemic/hyperinsulinemic clamp after 1-wk dietary control and a second clamp after completing the study.The study was performed at Ohio State University's General Clinical Research Center.There were 18 obese, mildly diabetic humans included in the study.Aerobic exercise training was performed for 7 d.Whole-body, peripheral, and hepatic insulin sensitivity were measured.Exercise training did not have an impact on peripheral glucose uptake or endogenous glucose production during the basal state or low-dose insulin. Likewise, it did not alter endogenous glucose production during high-dose insulin. However, 1-wk of exercise training increased both whole-body (P0.05) and peripheral insulin sensitivity (P0.0001) during high-dose insulin.Improvements to whole body insulin sensitivity after short-term aerobic exercise training are due to gains in peripheral, not heptic insulin sensitivity.

Objective: We studied plasma adiponectin, insulin sensitivity, and insulin secretion before and after oral glucose challenge in normal glucose tolerant, impaired glucose tolerant, and type 2 diabetic first degree relatives of African-American patients with type 2 diabetes. Research Methods and Procedures: We studied 19 subjects with normal glucose tolerance (NGT), 8 with impaired glucose tolerance (IGT), and 14 with type 2 diabetes. Serum glucose, insulin, C-peptide, and plasma adiponectin levels were measured before and 2 hours after oral glucose tolerance test. Homeostasis model assessment-insulin resistance index (HOMA-IR) and HOMA-β cell function were calculated in each subject using HOMA. We empirically defined insulin sensitivity as HOMA-IR 2.68. Results: Subjects with IGT and type 2 diabetes were more insulin resistant (as assessed by HOMA-IR) when compared with NGT subjects. Mean plasma fasting adiponectin levels were significantly lower in the type 2 diabetes group when compared with NGT and IGT groups. Plasma adiponectin levels were 2-fold greater (11.09 ± 4.98 vs. 6.42 ± 3.3811 μg/mL) in insulin-sensitive (HOMA-IR, 1.74 ± 0.65) than in insulin-resistant (HOMA-IR, 5.12 ± 2.14) NGT subjects. Mean plasma adiponectin levels were significantly lower in the glucose tolerant, insulin-resistant subjects than in the insulin sensitive NGT subjects and were comparable with those of the patients with newly diagnosed type 2 diabetes. We found significant inverse relationships of adiponectin with HOMA-IR (r = −0.502, p = 0.046) and with HOMA-β cell function (r = −0.498, p = 0.042) but not with the percentage body fat (r = −0.368, p = 0.063), serum glucose, BMI, age, and glycosylated hemoglobin A1C (%A1C). Discussion: In summary, we found that plasma adiponectin levels were significantly lower in insulin-resistant, non-diabetic first degree relatives of African-American patients with type 2 diabetes and in those with newly diagnosed type 2 diabetes. We conclude that a decreased plasma adiponectin and insulin resistance coexist in a genetically prone subset of first degree African-American relatives before development of IGT and type 2 diabetes.

We examined the long-term metabolic effects of glipizide gastrointestinal therapeutic system (GITS), a potent sulfonylurea (SU), in impaired glucose-tolerant (IGT), first-degree relatives of African American patients with type 2 diabetes. To this end, we assessed glucose homeostasis, beta-cell function, insulin sensitivity (Si), and glucose effectiveness (Sg) in patients with IGT before and at yearly intervals for 24 months of GITS or an identical placebo in a randomized, double-blind manner. Eighteen IGT patients were randomized to receive either glipizide GITS (GITS, 5 mg/d, n = 9; mean age, 43.3 +/- 8.7 years; mean body mass index [BMI], 32.9 +/- 6.3 kg/m(2)) or identical placebo (PLAC, n = 9; mean age, 41.5 +/- 5.7 years; mean BMI, 39 +/- 4.2 kg/m(2)) for 24 months. Each of the subjects underwent oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FSIGT) at baseline and yearly intervals for 2 years. Si and Sg were determined by Bergman's minimal model method. The ability of beta cell to compensate for peripheral insulin resistance was calculated as the disposition index (DI). Chronic administration of glipizide GITS attenuated serum glucose responses to oral glucose challenge at 12 and 24 months when compared to baseline (0 months). In contrast, serum glucose levels at fasting and during OGTT tended to increase in the IGT/PLAC group at 12 and 24 months when compared to baseline. Serum insulin (P

The objective of this study was to examine the relationships among insulin and insulin sensitivity and risk factors for cardiovascular diseases in native Ghanaians with and without hypertension.We measured the anthropometric parameters, systolic and diastolic blood pressure, fasting serum triglycerides, cholesterol and high-density lipoprotein cholesterol and fasting and stimulated glucose, insulin and C-peptide of 200 Ghanaian subjects, who were between 25 to 74 years of age, and residing in the Accra Metropolitan area. Serum glucose, C-peptide and insulin concentrations were measured at baseline (fasting) and also 2 h after 75 gm oral glucose drink. Homeostasis model assessment was used to measure insulin resistance. Hypertension was defined as a blood pressure higher than 140/90 mmHg.There were 53 subjects with hypertension (HBP) and 147 subjects with normal blood pressure (NBP). The mean BMI, waist circumference and waist-to-hip circumference ratio for HBP and NBP subjects were 27.4+/-0.8, 24.8+/-0.4 kg/m(2); 89.8+/-11.7, 81.1+/-0.9 cm; and 0.87+/-0.08, 0.82+/-0.08 respectively, (p0.05). The fasting and 2-h plasma glucose concentrations in HBP and NBP subjects were 5.5+/-0.2, 7.2+/-0.3 mmol/l and 5.2+/-01, 6.8+/-0.2 mmol/l respectively (p0.05). The corresponding fasting and 2-h insulin concentrations were 10.0+/-0.7, 8.0+/-0.4 uU/ml and 47.3+/-3.7, 37.3+/-2.5 uU/ml respectively (p0.05). The insulin resistance index (HOMA-IR) in the HBP and the NBP groups were 2.49+/-0.2 and 1.95+/-0.13 (p0.05). The two groups had similar fasting and stimulated C-peptide, lipids and HDL concentrations. Correlations were found between blood pressure and the concentrations of lipids, HDL, fasting and stimulated insulin and C-peptide, and between fasting insulin and HOMA-IR with lipids and HDL concentrations. On multiple regression analysis, fasting insulin and HOMA-IR did not influence blood pressure variations significantly.We found clustering of hyperinsulinaemia, insulin resistance and truncal obesity in hypertensive Ghanaian subjects but dissociation between insulin resistance, hypertension and atherogenic lipid and lipoprotein profile.

The increasing prevalence and incidence of diabetes and its long-term complications in sub-Saharan Africa (SSA) could have devastating human and economic toll if the trends remain unabated in the future. Approximately 90% or majority of patients with diabetes belongs to the adult onset, type 2 diabetes category while 10% have type 1 diabetes in SSA. However, because of the paucity of metabolic and clinical data, a clear understanding of the natural history of both diseases and the classification of diabetes subtypes has been hampered. Nevertheless, we have attempted to provide a concise review of the pathophysiology of both type 1 and type 2 diabetes as well as phenotypic and clinical variations in patients residing in SSA. The limited metabolic data, (albeit increasing), from high-risk and diabetic individuals in the SSA, have contributed significantly to the understanding of the pathogenetic mechanisms of diabetes and the variations in the presentation of the disease. Sub-Saharan African patients with t...

To evaluate predictors of outcomes associated with an inpatient diabetes education and discharge support program for hospitalized patients with poorly controlled diabetes (glycated hemoglobin [HbA1c]9%).Patients participated in individualized diabetes education conducted by a certified diabetes educator (CDE) that included an exploration of barriers and goal setting during hospitalization with telephone follow-up and communication with primary providers at discharge. Predictors of HbA1c reduction, successful follow-up, and readmission were analyzed.There were 82 subjects, and 48% were insulin naïve. Patients with type 2 diabetes (T2D, n = 58) had a significant decrease in HbA1c at follow-up (-2.8%, P.0001), while those with type 1 diabetes (T1D, n = 19) did not (+0.02%, P = .96). However, after adjustment for other factors, only increasing age, higher baseline HbA1c, earlier education, and initiation of basal insulin were significant predictors of reduction in HbA1c. Higher area level income and empowerment and earlier education were significant predictors of outpatient follow-up within 30 days. While 28% were admitted for severe hyperglycemia, only 1 patient was readmitted with severe hyperglycemia. Successful phone contact was 77% and 57% with and without the support of non-CDE assistants respectively, but all outcomes were similar.The study suggests that an individualized inpatient diabetes education and transition program is associated with a significant reduction in HbA1c that is dependent on baseline HbA1c, older age, initiation of insulin, and earlier enrollment. Additional interventions are needed to ensure better continuity of care.

Healthcare providers managing older patients with type 2 diabetes mellitus (T2DM) face a complex milieu of medical conditions and comorbidities, which increase the risk of unintended treatment consequences. The objective of this study was to understand factors associated with hypoglycemia-related hospitalizations among adults with T2DM with an emphasis on older patients.A large retrospective cohort study using claims data from the United States was undertaken identifying actively registered patients diagnosed with T2DM and at least one diabetes medication prescription.The main outcomes included hypoglycemia-related hospitalization and frequency of comorbidities.Of patients with T2DM and hospitalization records (n = 887,182), 52.3% were male and 30.7% were aged ≥65 years. At baseline, the proportion of patients taking metformin was 52.4%, insulin 7.3%, and sulfonylurea 26.4%. Among those with diabetes-related hospitalizations, the incidence of hospitalization-related hypoglycemia in patients ≥65 years of age was greater than in patients65 years of age (0.59 compared to 0.16 per 1000 person years). Using boosted regression tree modeling, age (older vs. younger), sulfonylurea use, insulin use, and renal disease were variables most associated with predicting hospitalizations associated with hypoglycemia. Elderly patients prescribed both insulin and sulfonylurea were most likely to experience hypoglycemia-related hospitalizations (odds ratio = 4.7; 95% CI 3.7-6.1).Older patients using both insulin and sulfonylurea were most likely to experience a hypoglycemia-related hospitalization. Age, sulfonylurea use, insulin use, renal disease, a history of hypoglycemia-related hospitalization and general hospitalization were the leading variables associated with hypoglycemia-related hospitalization. Glucagon-like peptide and dipeptidyl peptidase-4 medication use was not significantly associated with hypoglycemia-related hospitalizations. The strength of this analysis, compared to similar studies, lies in the large and generalizable sample size and statistical methodology, which control for the interdependence of predictive variables. Limitations include lack of information, such as dietary intake and exercise habits, which are known to influence the rate of hypoglycemia in certain patients. Given the frequency of use of insulin and sulfonylurea in a population at risk for hypoglycemia (older patients with diabetes), care should be taken when balancing cost and efficacy against safety and increased risk of hospitalization due to hypoglycemia.

Previous studies have shown that elastic properties of the aorta decrease, while left atrial dimensions, the contribution of left atrial systole to left ventricular filling, and left ventricular mass increase with age. In most studies, however, aortic function, and ventricular and atrial parameters were performed in different populations, and thus, the earliest manifestation of aging in the cardiovascular system is not known. The present study was undertaken to define the earliest cardiovascular abnormality(ies) occurring in the cardiovascular system with age. Patients and Method: In 181 normotensive subjects (147 females and 34 males) age 22–64 years, left ventricular mass, volumes, function and work (echocardiography and blood pressure), left atrial volumes and stroke volume (biplane area-length method by echo), pulse wave velocity (PWV) (carotid to femoral artery, Doppler), and left atrial kinetic energy were measured simultaneously: left atrial kinetic energy = 1/2 mV2, where m = left atrial stroke volume × 1.06 (blood specific gravity), v = transmitral A wave velocity. Regression analyses were performed to correlate all measured cardiovascular parameters with age. Results: Pulse wave velocity (r = 0.51), left atrial kinetic energy (r = 0.42), and A wave velocity (r = 0.38) were correlated to age, while left ventricular mass, function and work were not. Multiple regression analysis among ten clinical and echocardiographic parameters demonstrated that only age contributed independently to pulse wave velocity; only age and pulse wave velocity were contributed independently to left atrial kinetic energy; and only age contributed independently to A wave velocity. Conclusions: The data demonstrate that age-related alterations in aortic function and left atrial work (left atrial kinetic energy) can be defined prior to changes in left ventricular structure and systolic function. Simultaneous studies of left atrial, left ventricular, and aortic function are required to better understand the effect of aging on the cardiovascular system.

The authors have previously demonstrated abnormalities in glucose and insulin metabolism in nondiabetic black American (BA) adults versus white American (WA) adults. Whether similar glucoregulatory alterations extend to BA adolescents remain unknown. In addition, obesity, a known risk factor for insulin resistance and hyperinsulinemia, occurs in a greater proportion of BA adults and children when compared to WA. The objective of the present study was to examine the differential effects of obesity on glucose homeostasis in BA and WA adolescents.We examined glucose homeostasis in BA and WA adolescents using oral glucose tolerance test (OGTT), intravenous glucose tolerance test (IVGTT), and [6,6-2H2]-glucose infusion. The study consisted of four age-, sex-, and pubertal stage-matched groups: 15 lean BA, 29 lean WA, 7 obese BA, and 9 obese WA.Both obese groups had significantly increased insulin and C-peptide area under the curve (AUC) during OGTT and IVGTT when compared to their same-race lean counterparts. During OGTT, obese BA demonstrated greater insulin and C-peptide when compared to obese WA. During IVGTT, first- and second-phase insulin were significantly greater in obese BA versus obese WA.In summary, BA adolescents demonstrated insulin resistance which is markedly exaggerated in the face of obesity when compared to WA adolescents, implying a differential impact for obesity on glucose homeostasis that is unique to the obese BA adolescent group. In conclusion, there is a need for early aggressive weight management in obese BA adolescents.

OBJECTIVE Gestational diabetes mellitus (GDM) and positive parental history of type 2 diabetes are predictors of the future development of type 2 diabetes in several populations. However, the relative importance of parental history of diabetes and/or history of GDM as risk factors for the pathogenesis of diabetes in African-Americans remains unknown. Thus, the objectives of the present study were 1) to characterize the glucose homeostatic regulations and 2) to examine the contribution of parental history of type 2 diabetes to the potential metabolic alterations found in nondiabetic African-American women with a history of GDM (HGDM). RESEARCH DESIGN AND METHODS We evaluated β-cell secretion, insulin sensitivity (SI), and glucose-dependent glucose disposal (SG) in 15 glucose-tolerant African-American women with a parental history of type 2 diabetes and prior GDM (HGDM) and 35 women with a parental history of type 2 diabetes but without prior GDM (NHGDM). Fifteen healthy nonobese nondiabetic subjects without a family history of diabetes served as control subjects. Body composition was determined by bioelectrical impedance analyzer, and body fat distribution pattern was determined by waist-to-hip ratio (WHR). Insulin-modified frequently sampled intravenous glucose tolerance (FSIGT) test was performed in each subject. SI and SG were determined by the minimal model method. RESULTS The mean age, BMI, percent body fat content, and lean body mass were not different between the subgroups of relatives with and without a history of GDM, but were greater than those of the healthy control subjects. Mean fasting and postchallenge serum glucose levels were slightly but significantly greater in the HGDM versus NHGDM subjects and the healthy control subjects. However, the 2-h glucose levels were greater in the relatives with and without GDM when compared with the healthy control subjects. In contrast, mean postprandial serum insulin responses were significantly lower between t = 30 and 120 min in the HGDM versus NHGDM groups and the healthy control subjects. The mean serum insulin levels were not different in the NHGDM subjects and healthy control subjects. During the FSIGT test, acute first-phase insulin release (t = 0–5 min) was significantly lower in the HGDM versus NHGDM groups and healthy control subjects. Mean SI was significantly (P < 0.05) lower in the HGDM versus NHGDM subjects and healthy control subjects (1.87 ± 0.47 vs. 2.87 ± 0.35 and 3.09 ± 0.27 × 10−4 · min−1.[μU/ml]−1, respectively). SG was significantly lower in HGDM than NHGDM subjects and healthy control subjects (2.11 ± 0.15 vs. 3.25 ± 0.50 and 2.77 ± 0.22 × 10−2) · min−1, respectively). Mean glucose effectiveness at zero insulin concentrations (GEZI) was significantly lower in the HGDM subjects when compared with the NHGDM and healthy control subjects. CONCLUSIONS The present study demonstrates that in African-American women with a parental history of type 2 diabetes and GDM, defects in early-phase β-cell secretion, as well as a decreased SI, SG, and GEZI, persist when compared with those without GDM. We suggest that African-American women with a positive history of GDM have additional genetic defects that perhaps differ from that conferred by a parental history of diabetes alone. Alternatively, the metabolic and hormonal milieu during GDM may be associated with permanent alterations in β-cell function, SI, and glucose effectiveness in African-American women. These defects could play a significant role in the development of GDM, and perhaps in the subsequent development of type 2 diabetes, in African-American women.

Objective To describe two unusual cases of Cushing’s syndrome in a kindred with multiple endocrine neoplasia type I (MEN I). Methods The clinical and laboratory data as well as follow-up course of the two patients are reviewed in detail. Results Our first patient with a history of MEN I had hypercortisolism and computed tomographic evidence of a right adrenal mass (8.5 by 11 cm) extending into the inferior vena cava as well as multiple pulmonary nodules. He was diagnosed with Cushing’s syndrome attributable to metastatic adrenal cancer that progressed despite chemotherapy. He died 2 years later. His son, who was also diagnosed with MEN I, had adrenocorticotropic hormone-dependent Cushing’s syndrome. The plasma corticotropin-releasing hormone (CRH) level was high; magnetic resonance imaging showed normal pituitary findings but an islet cell tumor of the pancreas. The islet cell tumor was resected, and the patient’s urinary cortisol declined to upper limits of normal. CRH was detected in the tissue, and the patient was thought to have Cushing’s syndrome as a result of a CRH-secreting islet cell tumor. One year later, however, his Cushing’s syndrome recurred. Inferior petrosal sinus sampling suggested a pituitary source, and the patient underwent transsphenoidal hypophysectomy. Histopathologic examination did not reveal pituitary hyperplasia or microadenoma, but the patient was cured of his Cushing’s syndrome. Conclusion Cushing’s syndrome is a rare initial manifestation of MEN I. We report two unusual causes of Cushing’s syndrome in MEN I—that is, adrenal cancer and a probable CRH-secreting islet cell tumor. The natural history of Cushing’s syndrome in MEN I is not known; further studies should be conducted. (Endocr Pract. 1998;4:190-194)

OBJECTIVE The rate of type II diabetes in African-Americans is reaching epidemic proportions. African-Americans with type II diabetes suffer from more cardiovascular diseases (CVDs) associated with diabetes than the general population. Lower socioeconomic status (SES) and family history are often cited as contributory factors to the premature development of diabetes and CVDs in the general population. However, we are not aware of any study that has examined the relationships between SES and CVD risk factors (i.e., syndrome X) in a genetically enriched African-American population at high risk for type II diabetes. RESEARCH DESIGN AND METHODS We studied 200 healthy first-degree relatives of African-American patients with type II diabetes (age 25–65 years, mean 42.5 ± 8.4 years; 42 men, 158 women). Standard oral glucose tolerance test, metabolic, and anthropometric parameters, as well as questionnaires on SES, demographic characteristics, and physical activity, were obtained for each subject. SES was divided into quartiles based on annual income. To assess the impact of insulin on CVD risk, we examined clinical characteristics and metabolic parameters according to quartiles of fasting insulin concentrations. RESULTS Clinical characteristics, including mean age, BMI, waist-to-hip ratio (WHR), percentage body fat and lean body mass, and blood pressure were not statistically different among SES quartiles. There were no significant differences in any of the metabolic, blood pressure, lipid and lipoprotein, or anthropometric parameters among SES quartiles. When examined by insulin quartile, BMI, WHR, and body fat content tended to be greatest in the fourth quartile. Similarly, fasting and postprandial serum C-peptide and glucose levels were significantly higher in the fourth quartile. We observed greater levels of very low density lipoprotein (VLDL) cholesterol and triglycerides and lower levels of HDL cholesterol in the fourth compared with the first through third insulin quartiles. Serum cholesterol and LDL cholesterol were not associated with increasing insulin concentration assessed by quartiles. We found similar systolic and diastolic blood pressure, irrespective of insulin quartiles. We found relationships between fasting insulin and systolic blood pressure (r = 0.181, P < 0.05) and triglycerides (r = 0.247, P < 0.01), VLDL cholesterol (r = 0.237, P < 0.01), WHR (r = 0.268, P < 0.005), BMI (r = 0.308, P < 0.001), and percentage of body fat (r = 0.237, P < 0.01). CONCLUSIONS The present study demonstrates no SES/income effect on CVD risk factors or syndrome × in African-Americans at high risk for type II diabetes. Clustering of several components of syndrome × was seen in individuals in the highest quartiles compared with the lowest quartiles of insulin in our high-risk African-American population. We conclude that the well-established conventional risk factors for CVD in genetically enriched African-Americans are found only in individuals with the highest insulin levels, independent of SES.

Context: Insulin resistance is associated with altered vascular function in diabetes. Objective: The objective of the study was to define the overall and regional aortic function as well as the changes of aortic function over time in nondiabetic individuals with insulin resistance and a normal oral glucose tolerance test (OGTT). Design: This was a cross-sectional and longitudinal analysis with 12 months follow-up. Setting: The setting of the study was in primary care. Patients: Nondiabetic individuals (n = 181, mean age 42 ± 8 y) with a normal OGTT and insulin resistance as defined by the insulin sensitivity index (ISI) participated in the study. Interventions: ISI was estimated from serial measurements of plasma insulin and glucose during an iv glucose tolerance test. Ascending and abdominal aortic distensibility (AoD) and stiffness index-β (AoSI) were assessed using echocardiography. Carotid-to-femoral artery pulse wave velocity (PWVc-f; an index of overall aortic function) was measured from carotid and femoral arteries Doppler flow velocities recorded simultaneously with an electrocardiogram. Associations between ISI, AoD, AoSI, and PWVc-f were assessed using linear regression analyses and ANOVA. Differences between baseline and 12 months were compared using a paired t test. Main Outcome Measures: AoD and AoSI associations as well as changes over a 12-month period in relation to ISI were measured. Results: Ascending AoD (P = .01) and ascending AoSI (P = .025) were significantly associated with ISI; in contrast, abdominal AoD and AoSI and PWVc-f did not. Changes in AoD, AoSI, and PWVc-f over time were more prominent in individuals with low ISI compared with those with high ISI. Conclusions: The significant associations between ISI and aortic function suggest that insulin resistance may affect the cardiovascular system, even when OGTT is normal.

Obesity is a common component of non-insulin-dependent diabetes mellitus (NIDDM) and plays an important role in the development of insulin resistance and hyperinsulinemia. Prader-Willi syndrome (PWS) has been associated with morbid obesity and an increased propensity for early development of NIDDM. It has been assumed that the etiology for this increased rate of NIDDM is related to the morbid obesity and concomitant insulin resistance, but this remains controversial. To shed light on the glucoregulatory mechanisms in PWS, we studied both pediatric and adult PWS patients with normoglycemia. The objectives of our study were (1) to examine glucose, insulin, and C-peptide responses to oral (OGTT) and intravenous (IVGTT) glucose tolerance tests; (2) to characterize acute first- and second-phase insulin secretion during an IVGTT; (3) to assess hepatic insulin extraction (HIE) and insulin clearance (IC) in PWS subjects; and (4) to determine whether beta-cell function in PWS is age-dependent. These results in PWS were compared with values obtained in age-, sex-, and body mass index (BMI)-matched non-PWS obese controls. Three groups were studied. Group I consisted of nine PWS subjects under the age of 13 years and 22 age-, sex-, weight-, and puberty stage-matched obese subjects who underwent OGTT. Group II consisted of 14 adult PWS subjects and 10 age-, weight-, and BMI-matched obese adults who underwent OGTT. Group III consisted of nine adult PWS subjects and eight age-, sex-, and weight-matched obese adults who underwent frequently sampled IVGTT (FSIVGTT). During the OGTT in the pediatric group, fasting (86 +/- 3 v 89 +/- 2 mg/dL), peak (144 +/- 11 v 147 +/- 4 mg/dL), and total area under the curve (AUC) (6,984 +/- 1,320 v 6,963 +/- 615 mg/dL x min) glucose levels were not significantly different in PWS versus obese children, respectively. In contrast, fasting (20 +/- 6 v 37 +/- 4 microU/mL), peak (114 +/- 24 v 214 +/- 23 microU [correction of mU]/mL), and total AUC (12,673 +/- 2,176 v 26,734 +/- 2,608 microU/mL microU/mL min) insulin levels were significantly lower in pediatric PWS. During the OGTT in the adult groups, neither fasting insulin (16.7 +/- 2.8 v 13.5 +/- 2.5 microU/mL) nor total AUC for insulin (10,664 +/- 1,955 v 11,623 +/- 1,584 microU/mL x min) were significantly different in adult PWS and obese groups. During the IVGTT in adults, both first-phase (138 +/- 42 v 454 +/- 102 microU/mL x min) and second-phase (295 +/- 66 v 1,015 +/- 231 microU/mL x min) insulin release were significantly reduced in PWS subjects despite similar glucose levels. Similarly, first-phase (8.6 +/- 2.3 v 21 +/- 4.6 ng/dL x min) and second-phase (47 +/- 4.6 v 75 +/- 14 ng/dL x min) C-peptide responses were also significantly reduced in PWS subjects. In contrast, mean HIE and IC was 33% higher in PWS subjects versus obese controls (15.4 +/- 1.5 v 10.3 +/- 1.6). Similarly, poststimulation HIE and IC was significantly greater (5.2 +/- 0.8 v 2.4 +/- 0.4) in the PWS group compared with the obese group (P.01). In summary, this study demonstrates that nondiabetic PWS subjects manifest (1) a reduced beta-cell response to glucose stimulation, (2) a significantly increased HIE compared with obese controls, and (3) a dissociation of obesity and insulin resistance, in contrast to normal obese subjects. We conclude that glucoregulatory mechanisms are different in obese PWS versus non-PWS subjects.

The authors evaluated the significance of beta cell function, non-insulin-dependent glucose disposal (glucose effectiveness [Sg]), and insulin-dependent glucose disposal (insulin sensitivity) in African immigrants with varying degrees of glucose tolerance. Thirty-two African immigrants residing in Franklin County, Ohio, were studied. There were 16 subjects with normal glucose tolerance (NGT), 11 with intermediate glucose tolerance (IGT), and 5 with type II diabetes mellitus (DM). Insulin sensitivity index and Sg were measured by an insulin-modified, frequently sampled intravenous glucose tolerance test. The mean fasting and post-glucose serum glucose levels were lowest in the NGT, intermediate in the IGT group, and highest in the DM group. Mean serum insulin and c-peptide responses rose briskly by threefold to a peak in the NGT and the IGT groups. In the DM group, mean serum insulin and c-peptide responses were severely blunted to glucose stimulation. The sensitivity index was highest in the NGT (3.09 +/- 0.27), intermediate in the IGT (1.81 +/- 0.47), and lowest in the DM (0.48 +/- 0.28 x 10(-2).mins-1 (microU/ml)-1). The Sg was identical in the NGT (2.78 +/- 0.22) and IGT (2.78 +/- 0.27) groups but was slightly but not significantly lower in the DM (2.20 +/- 0.35 x 10(-2).mins-1). In addition, the glucose decay constant was not statistically different in the NGT (3.00 +/- 0.38) and IGT (2.25 +/- 0.19) group, but the mean values were significantly greater than in the patients with diabetes (0.78 +/- 0.15 percent/mins). The mean disposition index (sensitivity index X beta cell function as assessed by both insulin and c-peptide) was significantly greater in NGT than in the IGT (P0.05) and in the diabetic group (P0.001). In summary, the authors demonstrate that, in native African immigrants, type II diabetes is associated with significant reduction in beta cell function, insulin sensitivity, and glucose decay constant, but not in Sg. In patients with intermediate or impaired glucose tolerance, there is moderate insulin resistance and evidence of inadequate compensation by beta cell, but the Sg, the Sg at theoretical insulin concentration, and glucose decay constant remain normal. They conclude that, unlike other ethnic and racial groups, in glucose intolerant native African patients, alterations in Sg or non-insulin dependent glucose disposal (ie, tissue glucose sensitivity) do not appear to play a significant role in the impairment of glucose tolerance and type II diabetes in African immigrants.

The importance of hyperglycemia in the Intensive Care Unit (ICU) is well established. However, little is known regarding the clinical predictive value of acute hyperglycemic events. This report describes a graphical model that quantifies the correlation between momentum/stochastic indicators, acute hyperglycemia, and clinical events in chronic ICU patients. The model is based on previously described principles of graphical representations of biomedical parameter data. We hypothesize that acute hyperglycemic events are significantly associated with major clinical events and that the model described herein helps to better characterize and quantify this important relationship. The following core competencies are addressed in this article: Medical knowledge, Patient care, Practice-based learning and improvement, Systems-based practice. Republished with permission from: Stawicki SP, Schuster D, Liu JF, Kamal J, Erdal S, Gerlach AT, Whitmill ML, Lindsey DE, Thomas YM, Murphy C, Steinberg SM. Introducing the glucogram: Description of a novel technique to quantify clinical significance of acute hyperglycemic events. OPUS 12 Scientist. 2009;3:2-5.

BACKGROUND Obesity is often associated with high cardiovascular disease risk factors. Obesity is common in African American women. We investigated the characteristics of metabolically healthy and metabolically unhealthy overweight/obese African American women based on the presence of insulin resistance. MATERIALS/METHODS We studied 196 apparently healthy overweight/obese African American women with family history of type 2 diabetes. Waist circumference, fasting glucose, insulin, c-peptide, lipids and lipoproteins, and systolic and diastolic blood pressure were obtained in each subject. In addition, insulin sensitivity was calculated using Bergman's Minimal Model Method. We defined insulin-sensitive metabolically healthy African American women as individuals with insulin sensitivity greater than 2.7 x 10(-4) x min(-1) (uU/ mL)(-1) and insulin resistant, metabolically unhealthy as insulin sensitivity less than 2.7 x 10(-4) x min(-1) (uU/mL)(-1). RESULTS Thirty-three percent of our subjects were metabolically healthy African American women, while 67% were metabolically unhealthy African American women. The metabolically healthy subjects were significantly younger and less obese than the metabolically unhealthy subgroup. Mean fasting serum glucose, insulin, and c-peptide were significantly lower (P = .001) in the metabolically healthy than in metabolically unhealthy subjects. However, the mean blood pressures were within normal in both subgroups. Mean serum cholesterol (p < .05) and triglyceride (p < .001) levels were significantly lower, whereas high-density lipoprotein cholesterol (p < .03) was significantly higher in the metabolically healthy than in the metabolically unhealthy subjects. We found 25.5% of our subjects had metabolic syndrome (30.3% metabolically unhealthy and 15.6% metabolically healthy). CONCLUSION We concluded that: (1) despite obesity, metabolically healthy African American women appear to be less prone to type 2 diabetes and cardiovascular disease and (2) in view of the higher prevalence of metabolic syndrome, metabolically unhealthy African American women should be targeted for primary prevention of type 2 diabetes and cardiovascular disease.

The epidemic of obesity is known to contribute annually to 2.6 million deaths worldwide. [1] Excessive adiposity is the primary etiology of major metabolic diseases and related mortality. These deaths are attributed mainly to the comorbidities associated with obesity, including hypertension (HTN), cardiovascular disease (CVD), and diabetes mellitus (DM). The global escalation of childhood obesity is a matter of grave concern. Recent data have demonstrated a nearly fourfold rise in the prevalence of childhood obesity, making the pediatric age group the fastest growing subpopulation of obese individuals in this country. [1] Corresponding data examining global obesity trends demonstrate similar patterns worldwide with rates of overweight—defined as having a body mass index (BMI) greater that 25 kg/m2—occurring in 40% of men and 30% of women and rates of obesity (BMI≥30 kg/m2) at approximately 25%. [2] This condition can have far-reaching consequences on the physical and mental health of the young obese patients with many of these chronic diseases surging in childhood rather than adulthood. The normal BMI values used for defining overweight and obesity in adults cannot be extrapolated to the pediatric population as BMI is known to change with age and gender during childhood and adolescence. Center for Disease Control (CDC) BMI-for-age growth charts for girls and boys provide standard translation of a BMI number into a percentile with age and gender specific normograms. [3] Children with BMI equal to or exceeding the age-gender-specific 95th percentile are defined obese. Those with BMI equal to or exceeding the 85th but are below 95th percentiles are defined overweight. [4]

Beta cell hypersecretion is associated with the syndrome of hyperandrogenism, insulin resistance, and acanthosis nigricans. It is unknown whether concomitant alpha cell secretory dysfunction occurs in patients with this syndrome. The authors evaluated the gastroenteropancreatic hormones in four family members with varying degrees of the hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome. Gastroenteropancreatic hormones were measured during oral glucose tolerance test with and without subcutaneous octreotide injection. The study revealed that the administration of subcutaneous octreotide resulted in suppression of beta cell function (insulin and c-peptide) but had no effect or a delayed effect on alpha cell secretion (glucagon). Furthermore, the severity of glucagon abnormalities paralleled that of beta cell hypersecretion and the clinical and phenotypic manifestations of acanthosis nigricans in our four patients. We speculate that this alpha cell aberration could potentially be involved in the altered glucose homeostasis and perhaps the skin manifestations of this syndrome. Therefore, glucagon levels should be evaluated in the hormonal studies in patients with hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome.

To determine the effectiveness of an algorithm containing 1 of 3 initial subcutaneous doses of insulin detemir and flexible prandial and supplemental insulin aspart in stable patients who have undergone cardiac surgery and are being transitioned off intravenous insulin infusion.Patients were extubated, were not taking vasopressors, and were otherwise stable, requiring at least 1 unit per hour of intravenous insulin at least 48 hours after surgery. Patients were randomly assigned to once-daily insulin detemir at 50%, 65%, or 80% of intravenous basal insulin requirements and received insulin aspart according to carbohydrate intake. The dose of insulin detemir was adjusted daily over 72 hours.Eighty-two patients were included. The percentages of patients with an initial morning glucose concentration of 80 to 130 mg/dL were 36%, 63%, and 56% of patients at the 50%, 65%, and 80% doses, respectively (P = .12). However, the mean overall glucose value at 24 and 72 hours was similar between groups, and 86%, 93%, and 92% of patients in each group, respectively, achieved a mean glucose concentration of 80 to 180 mg/dL at 72 hours (P = .60). Hypoglycemia (glucose65 mg/dL) only occurred in the 65% group (21%) and the 80% group (12%) over the first 72 hours (P = .02 in the 50% group compared with the 65% and 80% groups combined) with 1 event of a glucose concentration less than 40 mg/dL in the 80% group. There was no loss of glycemic control by the end of the once-daily dosing interval.Glycemic targets can be achieved without hypoglycemia by 72 hours in most patients who have undergone cardiac surgery and require intravenous insulin with a regimen consisting of an initial insulin detemir dose of 50% of basal intravenous insulin requirements and prandial and supplemental insulin.

Obesity is an independent risk factor in trauma-related morbidity in adults. The purpose of this study was to investigate the effect of obesity in the pediatric trauma population.All patients (6-20 years) between January 2004 and July 2007 were retrospectively reviewed and defined as non-obese (body mass index [BMI]95th percentile for age) or obese (BMIor =95th percentile for age). Groups were compared for differences in demographics, initial vital signs, mechanisms of injury, length of stay, intensive care unit stay, ventilator days, Injury Severity Score, operative procedures, and clinical outcomes.Of 1314 patients analyzed, there were 1020 (77%) nonobese patients (mean BMI = 18.8 kg/m(2)) and 294 (23%) obese patients (mean BMI = 29.7 kg/m(2)). There was no significant difference in sex, heart rate, length of stay, intensive care unit days, ventilator days, Injury Severity Score, and mortality between the groups. The obese children were significantly younger than the nonobese children (10.9 +/- 3.3 vs 11.5 +/- 3.5 years; P = .008) and had a higher systolic blood pressure during initial evaluation (128 +/- 17 vs 124 +/- 16 mm Hg, P.001). In addition, the obese group had a higher incidence of extremity fractures (55% vs 40%; P.001) and orthopedic surgical intervention (42% vs 30%; P.001) but a lower incidence of closed head injury (12% vs 18%; P = .013) and intraabdominal injuries (6% vs 11%; P = .023). Evaluation of complications showed a higher incidence of decubitus ulcers (P = .043) and deep vein thrombosis (P = .008) in the obese group.In pediatric trauma patients, obesity may be a risk factor for sustaining an extremity fracture requiring operative intervention and having a higher risk for certain complications (ie, deep venous thrombosis [DVT] and decubitus ulcers) despite having a lower incidence of intracranial and intraabdominal injuries. Results are similar to reports examining the effect(s) of obesity on the adult population.

Obesity has reached epidemic proportions in the USA with a nearly fourfold rise in the prevalence of childhood obesity. There are many possible etiologies of obesity as the adipose tissue plays a significant, complex role in the physiology of fuel metabolism and hormone regulation. The development of obesity represents a pathophysiologic increase in fat mass in which multiple metabolic pathways are deranged. The consequences of these metabolic derangements, including insulin resistance and inflammation, are reflected in obesity-related comorbidities and can be seen in the setting of pediatric obesity. Obese adolescents demonstrate increased rates of early maturation, orthopedic growth abnormalities, diabetes mellitus, obstructive sleep apnea, hypertension, steatosis, and polycystic ovarian syndrome, placing this group of children at risk for long-term health problems and reduced quality of life. Given the negative short- and long-term impact of obesity on children, careful attention should be paid to the unique health issues of this "at-risk" population with both prevention and early intervention strategies.

African-American women (AAW) suffer disproportionately from hypertension and its consequences. We investigated the significance of systolic and diastolic blood pressure (SBP/DBP) as components of metabolic syndrome (MetS) in nondiabetic, overweight/obese AAW. We studied 258 AAW (mean age, 42.4 ± 8.4 years and body mass index (BMI), 33.4 ± 8.0 kg/m 2 ) in a cross-sectional manner. We estimated the prevalence of MetS and its components using Adult Treatment Panel (ATP III) criteria, insulin sensitivity (Si), insulin resistance (HOMA-IR), and cardiovascular disease risk factors according to the tertiles of blood pressure (BP). Mean age and BMI did not differ with increases in BP tertiles. At screening, 35.7% of our subjects were hypertensive. MetS was found in 32.2% of our AAW. Prevalence of MetS increased as the tertiles of BP increased (SBP = first [10.5%], second [15.1%], third [58.1%], and DBP=first [9.3%], second [23.3%], third [54.7%]). We found that the components of Adult Treatment Panel (ATP) did not track with the corresponding BP tertiles. However, the prevalence of individuals meeting ATP III criteria for BP was highest in the third tertile of both SBP and DBP. Consequently, the prevalence of MetS was highest in the third vs. first and second tertiles. Using linear regression analysis, SBP and DBP did not correlate with the conventional cardiovascular risk factors, HOMA-IR, or Si. In overweight/obese AAW, we found the components of MetS do not track with BP. In the absence of elevated BP, the prevalence of MetS appears to be very low in overweight and obese AAW. Conversely, elevated BP or hypertension was associated with remarkably higher rates of MetS in our AAW. Therefore BP criteria constitute an important and independent determinant of ATP III definition of MetS in AAW.

We aimed to identify whether racial differences in body composition and glucose metabolism occur in response to exercise and determine whether aerobic and resistance exercise modalities bring about differential changes in these parameters in African Americans and White persons with type 2 diabetes.Participants included 36 African American and 23 White men and women with type 2 diabetes who were randomly assigned to eight weeks of either resistance or aerobic exercise. Before and after this intervention, each participant underwent a series of measurements that assessed anthropometrics and glucose metabolism.African Americans responded more favorably to resistance training than did Whites. This difference was manifested by a significant improvement in BMI (-2.57%+/-.90% vs 2.57%+/-1.09%, P.01) and insulin resistance (-19.15%+/-9.00% vs 13.12%+/-11.86%, P.05) in African Americans compared to Whites. When comparing exercise modalities within the races, African Americans demonstrated a preferential response to resistance training.Eight weeks of resistance training by African Americans may have a more positive effect on weight loss and glucose metabolism than aerobic exercise training. Furthermore, the changes observed appear to be unique to African Americans, as no changes were observed in Whites after an equal amount of resistance training. When an exercise program is designed for a person with type 2 diabetes, race should be taken into consideration, and resistance exercise for African Americans may lead to increased weight loss and improved insulin sensitivity than does aerobic exercise.

Unique genetic traits appear to play a role in the increased rates of hypertension (HTN), glucose dysregulation/diabetes (T2DM), and obesity in persons of African descent. Indeed, with increasing rates of westernization/urbanization and concomitant increases in obesity and T2DM, a similar predisposition to the cardiometabolic syndrome and cardiovascular disease (CVD) can be seen in Africans compared with persons of African descent, with CVD reaching epidemic proportions in many areas of Africa. In addition, the complex relationships of metabolic abnormalities that are unique to individuals of African descent have also been demonstrated in Africans. These include: (1) a dissociation of HTN to insulin resistance; (2) relative favorable lipid profile in the setting of increasing rates of CVD; (3) low levels of visceral adiposity in the setting of obesity and insulin resistance; and (4) a dissociation of insulin sensitivity and adiponectin when compared with Caucasians. Although not well understood, these unique relationships suggest that conventional parameters for CVD do not apply to Africans of persons of African descent.

Objective: An association between glycosylated hemoglobin (GHb) and cardiovascular mortality in nondiabetic individuals has recently been reported. Prompt detection of nondiabetic individuals with high-normal GHb and early cardiovascular involvement may be of value for preventive strategies. In this investigation, a possible relationship between GHb, aortic function and left ventricular (LV) mass in nondiabetic individuals has been studied. Methods: A total of 263 nondiabetic African–Americans, aged 22–63 (mean 42 ± 8) years were studied. All individuals were first degree relatives of diabetic patients, had normal oral glucose tolerance test (2-h OGTT) and decreased peripheral action of insulin. LV diameters and mass (echocardiography); ascending and abdominal aortic distensibility (echocardiography, arterial pressure); pulse wave velocity (PWV; electrocardiography, Doppler); fasting glucose; GHb; insulin sensitivity index (SI) and 2-h OGTT were measured. Multiple linear and logistic regression analyses were used to identify significant independent associations of fasting glucose; GHb; SI and 2-h OGTT with aortic function and LV mass. Results: In fully adjusted multivariate logistic regression analysis, GHb predicted lower values of aortic distensibility (odds ratio (OR) 1.67 95% CI (1.04–2.75), P=0.04); higher PWV (OR 1.79 95% CI (1.09–2.93), P=0.022); and higher values of LV mass (OR 1.56 95% CI (1.08–2.88), P=0.029). Fasting glucose, SI, and 2 h OGTT were not associated with aortic function and LV mass. Conclusion: Higher GHb concentrations, even within ‘normal’ range, are independently associated with stiffer aorta and increased LV mass and thus may detect nondiabetic individuals at increased cardiovascular risk.

Peripheral insulin levels are determined by beta-cell secretion, insulin sensitivity, and hepatic insulin extraction (HIE). We have previously shown that whereas sulfonylureas reduce insulin extraction, metformin enhances HIE. However, the effects of thiazolidinediones (TZDs) on HIE remain uncertain. Thus, we investigated the potential contribution of hepatic insulin clearance to peripheral insulin levels during rosiglitazone therapy in African Americans with impaired glucose tolerance (IGT) and type 2 diabetes mellitus (DM). The study was composed of 12 first-degree relatives with IGT and 17 patients with newly diagnosed type 2 DM. Nineteen healthy relatives with normal glucose tolerance served as controls. Serum glucose, insulin, and C-peptide, and HIE (C-peptide-insulin molar ratios) were measured at t = 0 and 120 minutes during oral glucose tolerance test (OGTT) in all the subjects. The OGTT was performed before and after 3 months of rosiglitazone therapy (4 mg/d x 4 weeks and >8 mg/d x 8 weeks) in patients with IGT and type 2 DM. Insulin resistance index and beta-cell function were calculated in each subject using homeostasis model assessment (HOMA). Rosiglitazone therapy improved but did not normalize the overall glycemic control in the IGT and type 2 DM groups. After rosiglitazone therapy, the mean serum insulin and C-peptide levels at fasting remained unchanged. However, the 2-hour serum glucose and insulin were lower, whereas serum C-peptide was unchanged during 3 months of rosiglitazone treatment. Mean insulin resistance index of HOMA was reduced by 30% (4.12 +/- 1.95 vs 6.33 +/- 3.54, P < .05) in the type 2 DM group and by 21% (3.78 +/- 2.45 vs 4.81 +/- 3.49, P = NS) in the IGT group. Mean HIE values were significantly lower (70%) in the type 2 DM and IGT groups when compared with the normal glucose tolerance group. At 3 months, basal HIE was not significantly changed by rosiglitazone therapy in IGT and type 2 DM groups when compared with the baseline (0 month). However, rosiglitazone therapy was associated with increased HIE at 2 hours during OGTT by 40% and 30% in the IGT and type 2 DM groups, respectively, from the baseline (0 month) values. Furthermore, HIE inversely correlated with the insulin resistance index of HOMA (r = -.46, P < .05). We conclude that rosiglitazone therapy improved overall glucose tolerance and enhanced insulin sensitivity in patients with IGT and type 2 DM. Although basal HIE remained unchanged, rosiglitazone therapy increased postglucose challenge HIE in African Americans with IGT and type 2 DM. We speculate that TZDs increase insulin clearance or HIE after oral glucose challenge. This study suggests that in addition to insulin sensitization, rosiglitazone may be involved in insulin metabolism. The significance of the increased insulin clearance by TZD therapy remains uncertain and deserves further investigation in patients with insulin resistance and glucose intolerance.

Previous studies have shown that type 1 diabetes mellitus (DM) is associated with cardiovascular abnormalities. Early detection and treatment of these abnormalities may help to prevent the natural progression of the disease. The present study was undertaken to define early cardiovascular abnormalities in children with type 1 DM. Simultaneous evaluation of multiple cardiovascular parameters was performed in 14 children with type 1 DM and 14 age- and gender-matched normal subjects. Measurements of carotid artery intima-media thickness (cIMT, echocardiography), carotid and aortic (ascending and abdominal) distensibility (echocardiography, brachial artery blood pressure), aortic pulse wave velocity (carotid to femoral artery, Doppler), and left ventricular dimensions, mass, and function (echocardiography) were performed. Diabetic children demonstrated a greater cIMT (0.36 ±0.04 mm vs 0.31 ±0.03 mm, p=0.002) and decreased carotid artery distensibility (4.4 ±1.6 cm2·dynes-1·10-6 vs 6.0 ±1.9 cm2·dynes-1·10-6, p

We examined the metabolic effects of rosiglitazone therapy on glucose control, insulin sensitivity, insulin secretion, and adiponectin in first-degree relatives of African Americans with type 2 diabetes (DM) with impaired glucose tolerance (IGT) and DM for 3 months. The study was comprised of 12 first-degree relatives with IGT, 17 newly diagnosed DM, and 19 healthy relatives with normal glucose tolerance (NGT). Oral glucose tolerance test (OGTT) was performed before and after 3 months of rosiglitazone therapy (4 to 8 mg/d) in patients with IGT and DM. Serum glucose, insulin, C-peptide, and adiponectin levels were measured before and 2 hours during OGTT in the NGT and patients with IGT and DM. Insulin resistance index (HOMA-IR) and beta-cell function (HOMA-%B) were calculated in each subject using homeostasis model assessment (HOMA). Rosglitazone improved the overall glycemic control in the IGT and DM groups. Following rosiglitazone, the beta-cell secretion remained unchanged, while HOMR-IR was reduced in DM by 30% (4.12 +/- 1.95 v 6.33 +/- 3.54, P < .05) and the IGT group (3.78 +/- 2.45 v 4.81 +/- 3.49, P = not significant [NS]). Mean plasma adiponectin levels were significantly (P < .05) lower in the DM (6.74 +/- 1.95 microg/mL) when compared with the NGT group(9.61 +/- 5.09). Rosiglitazone significantly (P < .001) increased adiponectin levels by 2-fold in patients with IGT (22.2 +/- 10.97 microg/mL) and 2.5-fold greater in DM (15.68 +/- 8.23 microg/mL) at 3 months when compared with the 0 month. We conclude that adiponectin could play a significant role (1) in the pathogenesis of IGT and DM and (2) the beneficial metabolic effects of thiazolidinediones (TZDs) in high-risk African American patients.