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A global obesity pandemic is one of the most significant health threats worldwide owing to its close association with numerous comorbidities such as type 2 diabetes mellitus, arterial hypertension, dyslipidemia, heart failure, cancer and many others. Obesity and its comorbidities lead to a higher rate of cardiovascular complications, heart failure and increased cardiovascular and overall mortality. Bariatric surgery is at present the most potent therapy for obesity, inducing a significant weight loss in the majority of patients. In the long-term, a substantial proportion of patients after bariatric surgery experience a gradual weight regain that may, in some, reach up to a presurgical body weight. As a result, anti-obesity pharmacotherapy may be needed in some patients after bariatric surgery to prevent the weight regain or to further potentiate weight loss. This article provides an overview of the use of anti-obesity medications as an augmentation to bariatric surgery for obesity. Despite relatively limited published data, it can be concluded that anti-obesity medication can serve as an effective adjunct therapy to bariatric surgery to help boost post-bariatric weight loss or prevent weight regain. [ABSTRACT FROM AUTHOR]

Immune cells are an inseparable component of adipose tissue intimately involved in most of its functions. Physiologically, they regulate adipose tissue homeostasis, while in case of adipose tissue stress, immune cells are able to change their phenotype, enhance their count and subsequently contribute to the development and maintenance of local adipose tissue inflammation. Immune cells are an important sourc e of inflammatory cytokines and other pro-inflammatory products that further influe nce not only surrounding tissues but via systemic circulation also the whole organism being thus one of the main factors responsible for the transition from simple obesity to associated metabolic and cardiovascular complications. The purpose of this review is to summarize current knowledge on different adipose tissue immune cell subset s and their role in the development of obesity, type 2 diabetes mellitus and cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Dendritic cells (DCs) are professional antigen-presenting cells contributing to regulation of lymphocyte immune response. DCs are divided into two subtypes: CD11c-positive conventional or myeloid (cDCs) and CD123-positive plasmacytoid (pDCs) DCs. The aim of the study was to assess DCs (HLA-DR+ lineage-) and their subtypes by flow cytometry in peripheral blood and subcutaneous (SAT) and epicardial (EAT) adipose tissue in subjects with (T2DM, n=12) and without (non-T2DM, n=17) type 2 diabetes mellitus undergoing elective cardiac surgery. Subjects with T2DM had higher fasting glycemia (8.6±0.7 vs. 5.8±0.2 mmol/l, p<0.001) and glycated hemoglobin (52.0±3.4 vs. 36.9±1.0 mmol/mol, p<0.001) and tended to have more pronounced inflammation (hsCRP: 9.8±3.1 vs. 5.1±1.9 mg/ml, p=0.177) compared with subjects without T2DM. T2DM was associated with reduced total DCs in SAT (1.57±0.65 vs. 4.45±1.56% for T2DM vs. non-T2DM, p=0.041) with a similar, albeit insignificant, trend in EAT (0.996±0.33 vs. 2.46±0.78% for T2DM vs. non-T2DM, p=0.171). When analyzing DC subsets, no difference in cDCs was seen between any of the studied groups or adipose tissue pools. In contrast, pDCs were increased in both SAT (13.5±2.0 vs. 4.6±1.9% of DC cells, p=0.005) and EAT (29.1±8.7 vs. 8.4±2.4% of DC, p=0.045) of T2DM relative to non-T2DM subjects as well as in EAT of the T2DM group compared with corresponding SAT (29.1±8.7 vs. 13.5±2.0% of DC, p=0.020). Neither obesity nor coronary artery disease (CAD) significantly influenced the number of total, cDC, or pDC in SAT or EAT according to multiple regression analysis. In summary, T2DM decreased the amount of total dendritic cells in subcutaneous adipose tissue and increased plasmacytoid dendritic cells in subcutaneous and even more in epicardial adipose tissue. These findings suggest a potential role of pDCs in the development of T2DM-associated adipose tissue low-grade inflammation. [ABSTRACT FROM AUTHOR]

Immunocompetent cells including lymphocytes play a key role in the development of adipose tissue inflammation and obesity-related cardiovascular complications. The aim of the study was to explore the relationship between epicardial adipose tissue lymphocytes and coronary artery disease (CAD). To this end, we studied the content and phenotype of lymphocytes in peripheral blood, subcutaneous adipose tissue (SAT), and epicardial adipose tissue (EAT) in subjects with and without CAD undergoing elective cardiac surgery. Eleven subjects without CAD (non-CAD group) and 22 age-, BMI-, and HbA1C-matched individuals with CAD were included into the study. Blood, SAT, and EAT samples were obtained at the beginning of surgery. Lymphocyte populations were quantified as % of CD45+ cells using flow cytometry. Subjects with CAD had a higher total lymphocyte amount in EAT compared with SAT (32.24±7.45 vs. 11.22±1.34%, p=0.025) with a similar trend observed in non-CAD subjects (29.68±7.61 vs. 10.13±2.01%, p=0.067). T (CD3+) cells were increased (75.33±2.18 vs. 65.24±4.49%, p=0.032) and CD3- cells decreased (21.17±2.26 vs. 31.64±4.40%, p=0.028) in EAT of CAD relative to the non-CAD group. In both groups, EAT showed an elevated percentage of B cells (5.22±2.43 vs. 0.96±0.21%, p=0.039 for CAD and 12.49±5.83 vs. 1.16±0.19%, p=0.016 for non-CAD) and reduced natural killer (NK) cells (5.96±1.32 vs. 13.22±2.10%, p=0.012 for CAD and 5.32±1.97 vs. 13.81±2.72%, p=0.022 for non-CAD) relative to SAT. In conclusion, epicardial adipose tissue in subjects with CAD shows an increased amount of T lymphocytes relative to non-CAD individuals as well as a higher number of total and B lymphocytes and reduced NK cells as compared with corresponding SAT. These changes could contribute to the development of local inflammation and coronary atherosclerosis. [ABSTRACT FROM AUTHOR]

We performed a randomized controlled trial with the glucagon-like peptide-1 ( GLP-1) receptor agonist exenatide as add-on to standard peri-operative insulin therapy in patients undergoing elective cardiac surgery. The aims of the study were to intensify peri-operative glucose control while minimizing the risk of hypoglycaemia and to evaluate the suggested cardioprotective effects of GLP-1-based treatments. A total of 38 patients with decreased left ventricular systolic function (ejection fraction ≤50%) scheduled for elective coronary artery bypass grafting ( CABG) were randomized to receive either exenatide or placebo in a continuous 72-hour intravenous (i.v.) infusion on top of standard peri-operative insulin therapy. While no significant difference in postoperative echocardiographic variables was found between the groups, participants receiving exenatide showed improved peri-operative glucose control as compared with the placebo group (average glycaemia 6.4 ± 0.5 vs 7.3 ± 0.8 mmol/L; P < .001; percentage of time in target range of 4.5-6.5 mmol/L 54.8% ± 14.5% vs 38.6% ± 14.4%; P = .001; percentage of time above target range 39.7% ± 13.9% vs 52.8% ± 15.2%; P = .009) without an increased risk of hypoglycaemia (glycaemia <3.3 mmol/L: 0.10 ± 0.32 vs 0.21 ± 0.42 episodes per participant; P = .586). Continuous administration of i.v. exenatide in patients undergoing elective CABG could provide a safe option for intensifying the peri-operative glucose management of such patients. [ABSTRACT FROM AUTHOR]

Obesity is accompanied by the development of chronic low-grade inflammation in adipose tissue. The presence of chronic inflammatory response along with metabolically harmful factors released by adipose tissue into the circulation is associated with several metabolic complications of obesity such as type 2 diabetes mellitus or accelerated atherosclerosis. The present review is focused on macrophages and lymphocytes and their possible role in low-grade inflammation in fat. Both macrophages and lymphocytes respond to obesity-induced adipocyte hypertrophy by their migration into adipose tissue. After activation and differentiation, they contribute to the development of local inflammatory response and modulation of endocrine function of adipose tissue. Despite intensive research, the exact role of lymphocytes and macrophages within adipose tissue is only partially clarified and various data obtained by different approaches bring ambiguous information with respect to their polarization and cytokine production. Compared to immunocompetent cells, the role of adipocytes in the obesity-related adipose tissue inflammation is often underestimated despite their abundant production of factors with immunomodulatory actions such as cytokines or adipokines such as leptin, adiponektin, and others. In summary, conflicting evidence together with only partial correlation of in vitro findings with true in vivo situation due to great heterogeneity and molecular complexity of tissue environment calls for intensive research in this rapidly evolving and important area. [ABSTRACT FROM AUTHOR]

Duodenal-jejunal bypass liner (DJBL) is an endoscopically implantable device designed to noninvasively mimic the effects of gastrointestinal bypass operations by excluding the duodenum and proximal jejunum from the contact with ingested food. The aim of our study was to assess the influence of DJBL on anthropometric parameters, glucose regulation, metabolic and hormonal profile in obese patients with type 2 diabetes mellitus (T2DM) and to characterize both the magnitude and the possible mechanisms of its effect. Thirty obese patients with poorly controlled T2DM underwent the implantation of DJBL and were assessed before and 1, 6 and 10months after the implantation, and 3 months after the removal of DJBL. The implantation decreased body weight, and improved lipid levels and glucose regulation along with reduced glycemic variability. Serum concentrations of fibroblast growth factor 19 (FGF19) and bile acids markedly increased together with a tendency to restoration of postprandial peak of GLP1. White blood cell count slightly increased and red blood cell count decreased throughout the DJBL implantation period along with decreased ferritin, iron and vitamin B12 concentrations. Blood count returned to baseline values 3 months after DJBL removal. Decreased body weight and improved glucose control persisted with only slight deterioration 3 months after DJBL removal while the effect on lipids was lost. We conclude that the implantation of DJBL induced a sustained reduction in body weight and improvement in regulation of lipid and glucose. The increase in FGF19 and bile acids levels could be at least partially responsible for these effects. [ABSTRACT FROM AUTHOR]

The article offers information about the possible long-term effects of intermittent fasting when it comes to the reduction of microvascular diabetes complications. It discusses the application of the genetic model of severe type 2 diabetes leptin receptor–deficient db/db mice in an aim to study the effects of intermittent fasting versus ad libitum feeding in terms of long-term survival, metabolic parameters, and diabetic retinopathy.

Aim. In postcardiac surgery patients, we assessed the performance of a system for intensive intravenous insulin therapy using continuous glucose monitoring (CGM) and enhanced model predictive control (eMPC) algorithm. Methods. Glucose control in eMPC-CGM group (n = 12) was compared with a control (C) group (n = 12) treated by intravenous insulin infusion adjusted according to eMPC protocol with a variable sampling interval alone. In the eMPC-CGM group glucose measured with a REALTime CGM system (Guardian RT) served as input for the eMPC adjusting insulin infusion every 15 minutes. The accuracy of CGM was evaluated hourly using reference arterial glucose and Clarke error-grid analysis (C-EGA). Target glucose range was 4.4-6.1 mmol/L. Results. Of the 277 paired CGM-reference glycemic values, 270 (97.5%) were in clinically acceptable zones of C-EGA and only 7 (2.5%) were in unacceptable D zone. Glucose control in eMPC-CGM group was comparable to C group in all measured values (average glycemia, percentage of time above, within, and below target range,). No episode of hypoglycemia (<2.9 mmol) occurred in eMPC-CGM group compared to 2 in C group. Conclusion. Our data show that the combination of eMPC algorithm with CGM is reliable and accurate enough to test this approach in a larger study population. [ABSTRACT FROM AUTHOR]

Background: Metabolic syndrome (MS) is associated with increased risk of cardiovascular diseases and type 2 diabetes mellitus (DM2). Insulin resistance is one of the major mechanisms of developing of MS, but an equally important role in its pathogenesis is played by the white adipose tissue and substances it produces -- the adipokines. The aim of our study was to investigate the influence of major factors of the metabolic syndrome on plasma levels of adipokines (adiponectin, leptin) and gastrointestinal hormone ghrelin. Methods: We examined 153 patients (87 men) with average age of 58.9 years. In each patient the presence of MS components was assessed according to modified NCEP ATP III criteria, which include impaired glucose tolerance (IGT) or DM2, obesity, hypertriglyceridaemia and elevated blood pressure. Hormone plasma concentrations were measured using standard RIA (radioimmunoassay) methods. The influence of several MS components on these concentrations was then statistically analysed. Results: In our study we confirmed that a tendency to decreased adiponectin levels was associated with the presence of DM2 and elevated BMI, although these differences were not statistically significant. In males its values depended more on BMI and in females especially on DM2. Leptin levels were significantly increased in individuals with glucose metabolism disorders and this relation was more stressed in men. The values of ghrelin tended to rise according to BMI, especially in non-diabetic individuals. Conclusion: Levels of investigated hormones showed a relation to the major components of MS -- total obesity and glucose metabolism disorders connected with insulin resistance. Statistical significance of this relation was influenced by great interindividual variability, presumably caused by other factors of MS. Intersexual differences could most likely be contributed to different distribution of body fat -- gluteofemoral vs. abdominal obesity. [ABSTRACT FROM AUTHOR]

The aim of our study was to analyze mitochondrial and endoplasmic reticulum (ER) gene expression profiles in subcutaneous (SAT) and epicardial (EAT) adipose tissue, skeletal muscle, and myocardium in patients with and without CAD undergoing elective cardiac surgery. Thirty-eight patients, 27 with (CAD group) and 11 without CAD (noCAD group), undergoing coronary artery bypass grafting and/or valvular surgery were included in the study. EAT, SAT, intercostal skeletal muscle, and right atrium tissue and blood samples were collected at the start and end of surgery; mRNA expression of selected mitochondrial and ER stress genes was assessed using qRT-PCR. The presence of CAD was associated with decreased mRNA expression of most of the investigated mitochondrial respiratory chain genes in EAT, while no such changes were seen in SAT or other tissues. In contrast, the expression of ER stress genes did not differ between the CAD and noCAD groups in almost any tissue. Cardiac surgery further augmented mitochondrial dysfunction in EAT. In our study, CAD was associated with decreased expression of mitochondrial, but not endoplasmic reticulum stress genes in EAT. These changes may contribute to the acceleration of coronary atherosclerosis. [ABSTRACT FROM AUTHOR]

Introduction: Multiple daily injection insulin regimen (MDI) represents the most intensive insulin regimen used in the management of people with type 2 diabetes (PwT2D). Its efficacy regarding glycaemic control is counterbalanced by the increased risk of hypoglycaemia, frequently observed tendency to weight gain and necessity for frequent glucose monitoring. Recent introduction of novel antidiabetic medications with pleiotropic effects reaching far beyond the reduction of glycaemia (HbA1c), such as the glucagon-like peptide 1 receptor agonist (GLP-1 RA), has significantly widened the therapeutic options available for management of T2D. Consequently, there is currently a substantial number of PwT2D for whom the MDI regimen was initiated at a time when no other options were available. Yet, in present times, these individuals could benefit from simplified insulin regimens ideally taking advantage of the beneficial effects of the novel classes of antidiabetic medications. iGlarLixi (Suliqua®) is a once-daily fixed-ratio combination of basal insulin analogue glargine 100 U/ml and a GLP-1 RA lixisenatide. Methods: Insulin therapy DE-intensificAtion with iglarLixi (IDEAL) is a six-centre, open-label, parallel-group, active comparator, phase IV randomised controlled trial with a 24-week active treatment period examining the efficacy and safety of MDI regimen de-intensification with once-daily administration of iGlarLixi versus MDI regimen continuation in PwT2D on a backgroud therapy with metformin ± sodium-glucose cotransporter 2 inhibitor. Planned Outcomes: The primary objective is to compare the effects of MDI therapy de-intensification with iGlarLixi versus MDI regimen continuation regarding glycaemic control (HbA1c). Secondary objectives include detailed evaluation of the effects of MDI regimen de-intensification with iGlarLixi on glycaemic control using standardised continuous glucose monitoring (CGM) metrics and self-monitoring of plasma glucose. Furthermore, body weight and body composition analysis, quality of life and safety profile are evaluated. Trial Registration: ClinicalTrials.gov, identifier NCT04945070. [ABSTRACT FROM AUTHOR]

Background: Maternal diabetes adversely affects fetal cardiovascular system development. Previous studies have reported that the fetuses of mothers with diabetes exhibit both structural and functional changes; nevertheless, prior studies have not examined the association between glucose control and fetal cardiac morphology and performance. Thus, the objective was to determine the association between fetal cardiac morphology and function and maternal glucose control in type 1 diabetes and to compare the differences in measured cardiac parameters between the fetuses of mothers with diabetes and healthy controls. Methods: In this prospective, longitudinal case-control study — including 62 pregnant women with type 1 diabetes mellitus and 30 healthy pregnant women — fetal cardiac assessment using B-mode, M-mode, and spectral pulsed-wave Doppler was performed in the second and third trimesters. In women with T1DM, glycated hemoglobin and data obtained from glucose sensors — including the percentage of time in, below, and above the range (TIR, TBR, and TAR, respectively), and coefficient of variation (CV) — were analyzed across three time periods: the last menstrual period to 13 (V1), 14–22 (V2), and 23–32 weeks (V3) of gestation. Fetal cardiac indices were compared between groups, and the correlation between glucose control and fetal cardiac indices was assessed. Results: At 28–32 weeks, the fetuses of women with T1DM exhibited increased left ventricular end-diastolic length, relative interventricular septum thickness, right ventricular cardiac output, and pulmonary valve peak systolic velocity compared with healthy controls. At 18–22 weeks, pulmonary and aortic valve diameters, left and right ventricular stroke volumes, and left cardiac output inversely correlated with the CV and glycated hemoglobin levels at V1 and V2. Furthermore, at 28–32 weeks, pulmonary and aortic valve diameters, left ventricular stroke volume, cardiac output, and right/left atrioventricular valve ratio inversely correlated with the TBR at V1, V2, and V3. Moreover, diastolic functional parameters correlated with the TAR and glycated hemoglobin levels, particularly after the first trimester. Conclusion: In women with T1DM, maternal hyperglycemia during pregnancy correlates with fetal diastolic function, whereas glucose variability and hypoglycemia inversely correlate with fetal left ventricular systolic function in the second and third trimesters. Key message: This prospective longitudinal study demonstrates that in women with T1DM, maternal hyperglycemia during pregnancy correlates with fetal diastolic function. In contrast, glucose variability and hypoglycemia inversely correlate with fetal left ventricular systolic function in the second and third trimesters. [ABSTRACT FROM AUTHOR]

To determine the optimal week for labor induction in women with diet-controlled gestational diabetes mellitus by comparing differences in perinatal and neonatal outcomes of labor induction to expectant management at different gestational weeks. Methods: This was a retrospective analysis of a prospectively recruited cohort of 797 singleton pregnancies complicated by diet-controlled gestational diabetes mellitus that were diagnosed, treated, and delivered after 37 weeks in a tertiary, university-affiliated perinatal center between January 2016 and December 2021. Results: The incidence of neonatal complications was highest when delivery occurred at 37 weeks, whereas fetal macrosomia occurred mostly at 41 weeks (20.7%); the frequency of large for gestational age infants did not differ between the groups. Conversely, the best neonatal outcomes were observed at 40 weeks due to the lowest number of neonates requiring phototherapy for neonatal jaundice (1.7%) and the smallest proportion of neonates experiencing composite adverse neonatal outcomes defined as neonatal hypoglycemia, phototherapy, clavicle fracture, or umbilical artery pH < 7.15 (10.4%). Compared with expectant management, the risk for neonatal hypoglycemia was increased for induction at 39 weeks (adjusted odds ratio 12.29, 95% confidence interval 1.35–111.75, p = 0.026) and that for fetal macrosomia was decreased for induction at 40 weeks (adjusted odds ratio 0.11, 95% confidence interval 0.01–0.92, p = 0.041), after adjusting for maternal pre-pregnancy body mass index, nulliparity, and mean pregnancy A1c. Conclusions: The lowest rate of neonatal complications was observed at 40 weeks. Labor induction at 40 weeks prevented fetal macrosomia. [ABSTRACT FROM AUTHOR]

The relationship between Hashimoto’s thyroiditis (HT) and thyroid cancer (TC) is a controversial topic; it remains unclear if HT acts as a risk factor of TC. The aim of our study was to compare the presence of HT and thyroid function in patients with TC and benign nodules. We analyzed 2571 patients after fine needle aspiration biopsy of thyroid nodule. Totally, 91 patients with primary TC and 182 sex- and age-matched controls were included. Positive antithyroid peroxidase (anti-TPO) and antithyroglobulin (anti-Tg) antibodies were associated with TC (anti-TPO 44% in TC vs. 27% in controls, P=0.005, anti-TG 35% in TC group vs. 21% in controls, P=0.018), and the TC group had significantly higher TSH (median 1.88 mIU/l vs. 1.21 mIU/l, P<0.001). Using multiple logistic regression, positive anti-TPO was identified as an independent risk factor (OR 2.21, P=0.018), while spontaneously suppressed TSH<0.5 mIU/l was a protective factor (OR 0.3, P=0.01) against TC. In conclusion, nodules in subjects with positive antithyroid antibodies could be considered to have a higher risk of malignancy. However, based on our results, it is not possible to declare that TC is triggered by HT. [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus is defined as diabetes diagnosed in the second or third trimester of pregnancy in patients with no history of diabetes prior to gestation. It is the most common complication of pregnancy. The underlying pathophysiology shares some common features with type 2 diabetes mellitus (T2DM) combining relatively insufficient insulin secretion with increased peripheral insulin resistance. While a certain degree of insulin resistance is the physiological characteristics of the second half of pregnancy, it is significantly more pronounced in patients with gestational diabetes. Adipose tissue dysfunction and subclinical inflammation in obesity are well-described causes of increased insulin resistance in non-pregnant subjects and are often observed in individuals with T2DM. Emerging evidence of altered adipokine expression and local inflammation in adipose tissue in patients with gestational diabetes suggests an important involvement of adipose tissue in its etiopathogenesis. This review aims to summarize current knowledge of adipose tissue dysfunction and its role in the development of gestational diabetes. We specifically focus on the significance of alterations of adipokines and immunocompetent cells number and phenotype in fat. Detailed understanding of the role of adipose tissue in gestational diabetes may provide new insights into its pathophysiology and open new possibilities of its prevention and treatment. [ABSTRACT FROM AUTHOR]

Increasing worldwide prevalence of type 2 diabetes mellitus and its accompanying pathologies such as obesity, arterial hypertension and dyslipidemia represents one of the most important challenges of current medicine. Despite intensive efforts, high percentage of patients with type 2 diabetes does not achieve treatment goals and struggle with increasing body weight and poor glucose control. While novel classes of antidiabetic medications such as incretin-based therapies and gliflozins have some favorable characteristics compared to older antidiabetics, the only therapeutic option shown to substantially modify the progression of diabetes or to achieve its remission is bariatric surgery. Its efficacy in the treatment of diabetes is well established, but the exact underlying modes of action are still only partially described. They include restriction of food amount, enhanced passage of chymus into distal part of small intestine with subsequent modification of gastrointestinal hormones and bile acids secretion, neural mechanisms, changes in gut microbiota and many other possible mechanisms underscoring the importance of the gut in the regulation of glucose metabolism. In addition to bariatric surgery, less-invasive endoscopic methods based on the principles of bariatric surgery were introduced and showed promising results. This review highlights the role of the intestine in the regulation of glucose homeostasis focusing on the mechanisms of action of bariatric and especially endoscopic methods of the treatment of diabetes. A better understanding of these mechanisms may lead to less invasive endoscopic treatments of diabetes and obesity that may complement and widen current therapeutic options. [ABSTRACT FROM AUTHOR]

Aim: Human exposure to organic pollutants (some of them also called endocrine disruptors) can be associated with adverse metabolic health outcomes including type 2 diabetes. The goal of this study was to compare the urine levels of bisphenol A and phthalate metabolites in subgroups of patients with metabolic syndrome composed of patients with and without three important components of metabolic syndrome (hypertension, dyslipidemia and diabetes).Methods: We have investigated 24 hr urine samples of 168 patients with metabolic syndrome from the Metabolic Outpatient Department of General University Hospital in Prague. Using standard metabolic syndrome criteria, we classified patients as dyslipidemic (n=87), hypertensive (n=96), and type 2 diabetic (n=58). Bisphenol A and 15 metabolites of phthalates were evaluated in relation to creatinine excretion. Samples were analysed with enzymatic cleavage of glucuronide using ultra-high-performance liquid chromatography-electrospray ionization tandem mass spectrometry in one laboratory with external quality control.Results: Four metabolites, mono-n-butyl phthalate, mono-(2-ethyl-5-hydroxyhexyl) phthalate, mono-(2-ethyl-5-oxohexyl) phthalate, and mono-(2-ethyl-5-carboxypentyl) phthalate showed significantly higher levels in diabetic compared to non-diabetic patients (p<0.001, p=0.002, p=0.002, and p=0.005, respectively). The differences remained significant after adjustment to hypertension, dyslipidemia, age, and BMI. No difference was found between either the hypertensive and non-hypertensive or dyslipidemic and non-dyslipidemic patients. There was no significant relation of bisphenol A level to diabetes, hypertension, dyslipidemia, age, and BMI.Conclusions: Urine levels of four phthalate metabolites were significantly higher in type 2 diabetics independently on specified predictors. Phthalate levels can be in relation to beta cell dysfunction in type 2 diabetic patients but this study is not able to show if the relation is causal. [ABSTRACT FROM AUTHOR]

Incretin-based therapies either increase endogenous levels of glucagon-like peptide-1 by prolonging its half-life (DPP-4 inhibitors) or directly stimulate its receptor (glucagon-like peptide-1 analogues; GLP-1 RA). They are currently widely used for the treatment of patients with type 2 diabetes mellitus owing to good antidiabetic efficacy, low risk of hypoglycemia, and relatively few other side effects. They also offer potential additional benefits such as weight neutrality or weight loss, positive effects on blood pressure and lipid levels, and potential cardio- and neuroprotectivity. Some experimental and clinical studies have raised concerns with respect to potential cardiovascular and pancreatic side effects of these therapies such as increased risk of heart failure with DPP-4 inhibitors as well as acute pancreatitis and pancreatic cancer with both classes. The available data are at present not robust enough to enable firm conclusions regarding these potential associations. Nevertheless, some recent data suggest a possibility of slightly increased risk of acute pancreatitis with GLP-1 RAs while they do not indicate increased risk of pancreatic cancer. Ongoing cardiovascular outcome trials will shed more light on the possible cardioprotective effects of incretin-based therapies as well as on the possible interconnection of DPP-4 inhibitors and heart failure. [ABSTRACT FROM AUTHOR]

Background: Increased glycemic variability (GV) may be associated with diabetes complications. Our study assessed the relationship between microvascular complications (MVCs) and GV calculated from continuous glucose monitoring (CGM) data in type 1 diabetes patients. Subjects and Methods: Thirty-two patients with type 1 diabetes (16 with and 16 without MVC) participated in this cross-sectional study. Vibration perception threshold (VPT), microalbuminuria, and fundoscopy were used to detect MVC. CGM data were recorded for 2 weeks and analyzed using proprietary software. Total SD (SDT), coefficient of variation (CV), and mean amplitude of glycemic excursions (MAGE) were compared. Results: Patients with any MVC had significantly higher GV, calculated from CGM, than patients without MVC (SDT, 4.1±0.6 vs. 3.4±0.8 mmol/L [ P=0.010]; CV, 0.43±0.06 vs. 0.38±0.08 [ P=0.032]; MAGE, 6.9±1.2 vs. 5.9±1.2 mmol/L [ P=0.014]) but comparable glycated hemoglobin (HbA1c) (70±9 vs. 69±10 mmol/mol [8.6±0.8% vs. 8.5±0.9%], difference not significant). No significant difference in GV was found between the two groups when using only self-monitored blood glucose (SMBG) data. A positive association was found between VPT and SDT in all patients ( r=0.51, P=0.0026). Conclusions: Patients with type 1 diabetes and any MVC had significantly higher GV calculated from CGM, but not from SMBG, than patients with comparable glycemic control but without complications. This supports the hypothesis that increased GV might be associated with MVC in type 1 diabetes and that HbA1c may not describe diabetes control completely. [ABSTRACT FROM AUTHOR]