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Purpose: Effects of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) in type-2 diabetes mellitus (T2DM) with or without prior heart failure (HF) have been inconsistent across cardiovascular outcome trials. This study aimed to investigate the impact of HF history at baseline on cardiovascular effects of GLP-1 RAs in T2DM. Methods: PubMed, Embase, Web of Science, and clinical trial registries were searched for randomized controlled trials (RCTs) or post hoc analyses (≥ 24 weeks) reporting HF hospitalizations and/or cardiovascular death (HHF/CVD), major adverse cardiovascular events (MACE) comprising of cardiovascular death, myocardial infarction, and stroke in adults with T2DM with or without HF history (PROSPERO:CRD42022367633). Hazard ratios (HRs) in GLP-1RAs versus placebo arms were pooled together using the generic inverse variance method in fixed-effects model. Subgroup analysis was performed. Results: We identified 5 eligible studies, pooling data retrieved from six RCTs and 48,489 individuals with T2DM. On pooled analysis, GLP1RA treatment versus placebo significantly reduced risk of HHF/CVD in only T2DM without HF history (HR = 0.84; 95%CI, 0.77–0.91; I2 = 14%; p < 0.001), but not in those with HF history (HR = 0.96; 95%CI, 0.85–1.08; I2 = 14%; p = 0.4) (p-interaction < 0.1). GLP-1RAs reduced incident HHF in T2DM with or without HF history (HR = 0.89; 95%CI, 0.80–0.98; I2 = 41%; p < 0.05) (p-interaction = 0.28). Sensitivity analysis excluding REWIND trial accentuated the impact of baseline HF history on both HHF/CVD and HHF (p-interaction < 0.05). Benefits on MACE with GLP-1RAs were consistently seen in T2DM regardless of HF history (p-interaction = 0.8). Conclusion: GLP-1RAs consistently prevented HF hospitalizations and MACE in T2DM regardless of baseline HF history, whereas significant attenuation of benefits on composite HHF/CV death were observed in those with HF history. [ABSTRACT FROM AUTHOR]

Context A subset of polycystic ovary syndrome (PCOS) individuals also have type 2 diabetes (T2D); an unmet need to identify this subgroup exists. Objective We looked at the potential role of serum chemerin, a proinflammatory adipokine, in identifying dysglycemic PCOS. Methods A total of 93 PCOS and 33 healthy controls were classified, based on fasting and 2-hour plasma glucose levels (2hPGPG) and glycated hemoglobin A1c (HbA1c) (%) into normoglycemic (n = 34), dysglycemic (n = 33), and T2D (n = 26). Serum chemerin were measured by enzyme-linked immunosorbent assay. Homeostatic model 2 assessment of insulin resistance (HOMA-2IR) and homeostatic model 2 assessment of β-cell function (HOMA-2β) were computed using serum C-peptide. Results Metabolic syndrome was present in 9.7% (National Cholesterol Education Program) of PCOS. Waist circumference, body fat (%), 2hPGPG, and HbA1c levels were significantly higher in T2D group. Serum triglycerides/high-density lipoprotein cholesterol (TGs/HDL-c) ratio was increased in PCOS individuals with T2D; no significant changes in total cholesterol and LDL-c levels were seen. Serum chemerin levels were significantly higher (P <.001) in the PCOS group. Total body fat (%), 2hPGPG, HbA1c, and TG/HDL-c ratio correlated positively with chemerin levels. Serum chemerin levels correlated positively with HOMA2IR and negatively with HOMA-2β. On receiver operating characteristic curve analysis, a serum chemerin cutoff level of greater than 309.3 ng/mL differentiated PCOS individuals with dysglycemia from those without (sensitivity 85.71%, specificity 89.47%). The Cohen kappa test revealed a substantial agreement (P <.001) between chemerin cutoff and 2hPGPG levels greater than 200 mg/dL. The present study is arguably the first ever to define a serum chemerin cutoff to distinguish PCOS individuals with T2D from those without. Conclusion Elevated serum chemerin levels reliably identify PCOS individuals with dysglycemia. Further, longitudinal studies with larger samples are required to confirm this association. [ABSTRACT FROM AUTHOR]

Background and Aims To investigate the cardiovascular effects of sodium–glucose co-transporter-2 inhibitors (SGLT2i) with concomitant mineralocorticoid receptor antagonist (MRA) use in heart failure (HF) regardless of ejection fraction (EF) and explore the risk of MRA-associated adverse events in individuals randomized to SGLT2i vs. placebo. Methods PubMed/MEDLINE, Web of Science, Embase, and clinical trial registries were searched for randomized controlled trials/ post-hoc analyses evaluating SGLT2i in HF with or without MRA use (PROSPERO: CRD42023397129). The main outcomes were composite of first hospitalization or urgent visit for HF/cardiovascular death (HHF/CVD), HHF, and CVD. Others were all-cause mortality, composite renal and safety outcomes. Hazard ratios (HR)/risk ratios were extracted. Fixed-effects meta-analyses and subgroup analyses were performed. Results Five eligible studies were included, pooling data from 21 947 people with HF (type 2 diabetes mellitus, n = 10 805). Compared to placebo, randomization to SGLT2i showed a similar reduction in HHF/CVD and HHF in people who were or were not using MRAs [HHF/CVD: hazard ratio (HR) 0.75; 95% confidence interval (CI) 0.68–0.81 vs. HR 0.79; 95% CI 0.72–0.86; P -interaction =.43; HHF: HR 0.74; 95% CI 0.67–0.83 vs. HR 0.71; 95% CI 0.63–0.80; P -interaction =.53], with a suggestion of greater relative reduction in CVD in chronic HF people randomized to SGLT2i and using MRAs irrespective of EF (HR 0.81; 95% CI 0.72–0.91 vs. HR 0.98; 95% CI 0.86–1.13; P -interaction =.034). SGLT2i reduced all-cause mortality (P -interaction =.27) and adverse renal endpoints regardless of MRA use (P -interaction =.73) despite a higher risk of volume depletion with concomitant MRAs (P -interaction =.082). SGLT2i attenuated the risk of mild hyperkalaemia (P -interaction <.001) and severe hyperkalaemia (P -interaction =.051) associated with MRA use. Conclusions MRAs did not influence SGLT2i effects on the composite of HHF/CVD, HHF or all-cause mortality; however, findings hinted at a more pronounced relative reduction in CVD in chronic HF patients regardless of EF who were randomized to SGLT2i and receiving an MRA compared to those randomized to SGLT2i and not receiving MRAs. SGLT2i attenuated the risk of MRA-associated treatment-emergent hyperkalaemia. These findings warrant further validation in well-designed randomized controlled trials. [ABSTRACT FROM AUTHOR]

Aims: To pool the effects of sodium‐glucose cotransporter‐2 (SGLT2) inhibitors on gout and to investigate the association of these effects with baseline serum uric acid (SUA), SUA lowering, and underlying conditions, such as type 2 diabetes mellitus (T2DM)/heart failure (HF). Methods: PubMed, Embase, Web of Science, Cochrane Library and clinical trial registry websites were searched for randomized controlled trials (RCTs) or post hoc analyses (≥1‐year duration; PROSPERO:CRD42023418525). The primary outcome was a composite of gouty arthritis/gout flares and commencement of anti‐gout drugs (SUA‐lowering drugs/colchicine). Hazard ratios (HRs) with 95% confidence interval (CI) were pooled using a generic inverse‐variance method with a random‐effects model. Mixed‐effects model univariate meta‐regression analysis was performed. Results: Five RCTs involving 29 776 patients (T2DM, n = 23 780) and 1052 gout‐related events were identified. Compared to placebo, SGLT2 inhibitor use was significantly associated with reduced risk of composite gout outcomes (HR 0.55, 95% CI 0.45‐0.67; I2 = 61%, P < 0.001). Treatment benefits did not differ between trials being conducted exclusively in baseline HF versus those conducted in patients with T2DM (P‐interaction = 0.37), but were greater with dapagliflozin 10 mg and canagliflozin 100/300 mg (P < 0.01 for subgroup differences). Sensitivity analysis excluding trials that evaluated the effects of empagliflozin 10/25 mg (HR 0.68, 95% CI 0.57‐0.81; I2 = 0%) accentuated the benefits of SGLT2 inhibitors with no between‐trial heterogeneity (HR 0.46, 95% CI 0.39‐0.55; I2 = 0%). Univariate meta‐regression found no impact of baseline SUA, SUA lowering on follow‐up, diuretic use, or other variables on their anti‐gout effects. Conclusion: We found that SGLT2 inhibitors significantly reduced the risk of gout in individuals with T2DM/HF. Lack of an association with SUA‐lowering effects suggests that metabolic and anti‐inflammatory effects of SGLT2 inhibitors may predominantly mediate their anti‐gout benefits. [ABSTRACT FROM AUTHOR]

Traditionally, treatment for type 2 diabetes (T2D) centered on the failure of insulin secretion from the beta cells of the pancreas and insulin resistance. Though effective in certain respects, these treatments are marred by multiple undesirable side effects. The discovery of the incretin defect and the role of glucagon in T2D shifted the focus to therapies that addressed not only the beta cell defect but also the alpha cell defect in the pancreas. Therapies addressing these defects, simultaneously, have switched the entire focus of T2D therapy by not only improving glycemic control but also reducing the risk of hypoglycemia and weight gain and improving outcomes. These newer modalities of treatment started off with dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 receptor agonists (GLP1-RAs), and now further treatments in the form of twincretins (GLP1/GIP dual agonists) and triple agonists (GLP1/GIP/glucagon agonists) are unraveling. This article provides a summary of the evidence available with these newer antidiabetics, which address the glucagon defect in T2D. [ABSTRACT FROM AUTHOR]

Background: Individuals with Turner syndrome (TS) have a high risk for prediabetes/type 2 Diabetes Mellitus (T2DM). There is scarce data regarding risk factors for prediabetes in TS, specially from South Asia. Methods: We conducted a cross-sectional study on girls with TS aged 12-30 years who had achieved pubertal stage B3 and above--spontaneously or with oestrogen. Anthropometric measurements and biochemical tests were conducted, and medical records were reviewed for details about pubertal onset and progression, growth hormone (GH) and oestrogen therapy. Results: Out of 129 patients with TS in our database, 99 met the criteria for inclusion, mean age 18.33+/-3.78 years and mean BMI 20.57+/-3.71 kg/m2. Prevalence of prediabetes was 23.23%. Plasma-glucose measured after 75 g-oral-anhydrous-glucose-load (OGTT-PPG) identified five additional prediabetes cases, who had normal fasting plasma glucose (FPG) or HbA1c%. Compared to those without prediabetes, TS with prediabetes (n = 23) had higher mean body weight, BMI, waist circumference (WC) [42.02+/-5.83 vs 36.22+/-8.07, 22.77+/-2.78 vs 19.91+/- 3.72, 85.26+/- 3.52 vs 81.08+/- 4.59, pall < 0.03], higher median WC-to-height ratio (WHtR) and WC-to-hip ratio (WHR) ((0.64 [0.6-0.69] vs 0.59[0.56- 0.66], 0.9[0.84-1.12] vs 0.85[0.75-1.01], pboth < 0.02), and higher LDL-cholesterol, triglycerides, and greater prevalence of hepatosteatosis (47.1% vs 21.1%, P < 0.01). Among GH recipients (n = 36), those with prediabetes had delayed initiation and shorter duration of GH therapy. There were no differences in cardiometabolic parameters or the prevalence of diabetes between different karyotypic variants of TS. BMI, WC and WHR had significant positive correlation with FBG, OGTT-PPG and HbA1c% (pall < 0.004). Delay in oestrogen initiation had a significant correlation with OGTT-PPG (Spearman's-rho = 0.69, P < 0.004). BMI, WHR and pubertal status were independent predictors for prediabetes (OR: 1.27 [1.03-1.57]), 1.18 [1.04-1.34]) and 0.09[0.02-0.38], respectively, pall < 0.02), but karyotype was not. BMI had the highest sensitivity [cut-off: 21.04 kg/m2 (sensitivity: 82.6%, specificity: 62.2%) and WHR had the highest specificity [cut-off: 0.89 (sensitivity: 73.9%, specificity 78.4%)] for predicting prediabetes. Conclusion: Indian girls with TS have a high risk for prediabetes, irrespective of underlying karyotype and should be screened with oral glucose challenge to identify prediabetes. Timely intervention against central obesity and early initiation of GH and oestrogen should be ensured in TS. Late presenting girls should be closely monitored for dysglycaemia before and during treatment with GH and/or oestrogen. [ABSTRACT FROM AUTHOR]

Purpose: To collate the effect of SGLT2 inhibitors (SGLT2i) on adverse gout events in people with type 2 diabetes mellitus (T2DM). Methods: PubMed/MEDLINE, Embase, and Web of Science databases were systematically searched using appropriate keywords/MeSH/Emtree terms till January 25, 2022, to identify observational studies, randomized controlled trials (RCTs) or post hoc analysis reporting incident gout events and/or commencement of anti-gout drug in people with T2DM receiving SGLT2i versus those not receiving SGLT2i. Subgroup analyses were performed using comparators as placebo/other antidiabetic drugs and presence/absence of baseline hyperuricemia (uric acid ≥ 7 or < 7 mg/dl). Hazard ratios (HR) with 95% confidence intervals (CI) were calculated. Results: We identified 5 studies (3 observational, 2 post hoc analysis of RCTs) pooling data retrieved from 568,010 people with T2DM. Pooled analysis showed that SGLT2i use was associated with 30% reduction in incident gout events/gout flares (HR 0.70, 95% CI: 0.59, 0.84, p < 0.001, I2 = 84%). Sensitivity analysis after excluding the retrospective observational study showed similar estimates (HR 0.65, 95% CI: 0.60, 0.70, p < 0.001, I2 = 0%). Subgroup analysis of data retrieved only from RCTs also showed significant benefits (HR 0.74, 95% CI: 0.55, 0.98, p = 0.03, I2 = 0%). Pooled analysis of data from 2 studies showed that SGLT2i use led to a significant reduction in the need for commencement of new anti-gout drug (pooled HR 0.58, 95% CI: 0.48, 0.71, p < 0.001, I2 = 0%). Consistent benefits were also observed for subgroup without baseline hyperuricemia (pooled HR 0.65, 95% CI: 0.47, 0.89, p < 0.01, I2 = 0%). Conclusions: SGLT2i may potentially prevent gout-related adverse events in people with T2DM. [ABSTRACT FROM AUTHOR]

Among all of the Super Elongation Complex (SEC) components, ELL1 (also known as ELL) is the only bona fide elongation factor that directly stimulates transcription elongation by RNA polymerase II. However, the mechanism(s) of functional regulation of ELL1 (referred to as ELL hereafter), through its stabilization, is completely unknown. Here, we report a function of human DBC1 in regulating ELL stability involving HDAC3, p300, and Siah1.Mechanistically, we showthat p300- mediated site-specific acetylation increases, whereas HDAC3-mediated deacetylation decreases, ELL stability through polyubiquitylation by the E3 ubiquitin ligase Siah1. DBC1 competes with HDAC3 for the same binding sites on ELL and thus increases its acetylation and stability. Knockdown of DBC1 reduces ELL levels and expression of a significant number of genes, including those involved in glucose metabolism. Consistently, Type 2 diabetes patient-derived peripheral blood mononuclear cells show reduced expression of DBC1 and ELL and associated key target genes required for glucose homeostasis. Thus, we describe a pathway of regulating stability and functions of key elongation factor ELL for expression of diverse sets of genes, including ones that are linked to Type 2 diabetes pathogenesis. [ABSTRACT FROM AUTHOR]

Introduction: Ankle Brachial Index (ABI), a useful tool in diagnosingperipheral arterial disease (PAD), maygive falsely high values in sclerosed & calcified arteries. Toe Brachial Index (TBI) offers an alternative approach here, as digital arteries are unaffected by atherosclerotic changes and medial calcification. Aim: To find out the sensitivity and specificity of ABI and TBI in diagnosing PAD in T2D compared to CT angiography (CTA) as a non-invasive gold standard. Methods: 175 subjects with T2D, >50 years or >40 yearswith diabetes duration >10 years, were included. ABI&TBI were measured with an automated vascular Doppler XT 6 ports (Hadeco Inc. Japan). ABI < 0.9 & TBI < 0.6 was considered abnormal. USG Color Doppler& CTA of lower limb arterial system was performed. Arterial stenosis >50% on CTA was taken as evidence of PAD. Statistical analysis was performed by using IBM-SPSS statistics version 26 & GraphPad Prism Software version 9.0e. Results: Theprevalence of PAD was 24%. The sensitivity& NPV of 38% and 80% respectively for ABI (<0.9) reflect an increased risk of failure to diagnose existing disease. The sensitivity of TBI was 90% indicating that TBI was quite likely to accurately detect PAD. The specificity of ABI and TBI were 90% and 85% respectively suggesting both were relatively unlikely to falsely detect PAD. ROC analysis showed ABI at 0.9950 has sensitivity 60% and specificity 70%, TBI at 0.6 has sensitivity 88% & specificity 86%. Conclusion: The prevalence of PAD in T2D is much higher in our study population compared to previous studies. We showed, TBI has much greater sensitivity and comparable specificity to ABI in participants at risk of PAD making it a useful tool for vascular assessment in people with T2D. The existing TBI cutoff is satisfactory and the ABI cutoff needs to be re-evaluated.{Table 1} [ABSTRACT FROM AUTHOR]

The authors comment on an article by E. Lontchi-Yimagou and colleagues in which they describe diabetes in individuals with low body mass index (BMI) from India. Topics discussed include comparison between type 2 diabetes (T2D) in White Caucasians and T2D in Asian Indians, metabolic characteristics of lean diabetes noted by Lontchi-Yimagou and colleagues, and criteria needed for individuals with diabetes to be grouped into a specific diagnostic category.

A letter to the editor on metabolic surgery for type 2 diabetes patients in Asia is presented.

Objective: To compare the clinical profile of long-term survivors and nonsurvivors with type 1 diabetes (T1D) in India. Research Design and Methods: This is a retrospective study of 76 individuals with T1D who had survived for at least 40 years ("survivors") and 51 individuals with T1D who had died with shorter duration of diabetes ("non-survivors"), from diabetes clinics in different cities of India. Prevalence of complications in both groups and causes of death of the nonsurvivors were analyzed. Retinopathy was diagnosed by retinal photography; chronic kidney disease (CKD) by urinary albumin excretion (micro-or macroalbuminuria) and estimated glomerular filtration rate; peripheral vascular disease (PVD) by doppler measurement of ankle-brachial pressure index; coronary artery disease (CAD) based on history of myocardial infarction or coronary revascularization, and neuropathy by biothesiometry. Results: Mean glycated hemoglobin (8.4% ± 1.5% vs. 10.7% ± 2.2%, P < 0.001), serum low-density lipoprotein cholesterol (91 ± 29 mg/dL vs. 107 ± 22 mg/dL, P = 0.004), and systolic blood pressure (135 ± 16 mmHg vs. 153 ± 37 mmHg, P = 0.003) were lower, and high-density lipoprotein cholesterol (51 ± 11 mg/dL vs. 43 ± 15 mg/dL, P = 0.002) higher, among survivors compared to nonsurvivors. Diabetic retinopathy, CKD, neuropathy, PVD, and CAD were more frequent among nonsurvivors. CAD [25.5%] and renal failure [23.5%] were the most frequent causes of death. Conclusions: In this first report of long-term survivors with T1D from India, we report that survivors had better glycemic and blood pressure control, more favorable lipid profiles and lower prevalence of complications compared to nonsurvivors. However, there could be other protective factors as well, which merit further studies. [ABSTRACT FROM AUTHOR]

Background: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and elevated risk of cardiovascular disease and diabetes. Chronic inflammation has been observed in PCOS in several studies but there is also opposing evidence and a dearth of research in Indians. Objective: To estimate chronic inflammation in PCOS and find its relationship with appropriate anthropometric and biochemical parameters. Materials and Methods: Chronic inflammation was assessed in 30 women with PCOS (Group A) and 30 healthy controls (Group B) with highly sensitive C-reactive protein (hsCRP), interleukin-6 (IL-6), tumour necrosis factor alpha (TNFα), and platelet microparticles (PMP). In group A, the relationship of chronic inflammation with insulin resistance, waist hip ratio (WHR) serum testosterone, and serum glutamate pyruvate transaminase (SGPT) were examined. Results: In group A, the hsCRP, TNFα, and PMP were significantly elevated compared to group B. However, IL-6 level was similar between the groups. In group A, PMP showed a significant positive correlation with waist-hip ratio and serum testosterone. IL-6 showed a significant positive correlation with insulin sensitivity and significant negative correlation with insulin resistance and serum glutamate pyruvate transaminase. Conclusion: PCOS is associated with chronic inflammation and PMP correlates positively with central adiposity and biochemical hyperandrogenism in women with PCOS. [ABSTRACT FROM AUTHOR]

Islets of type 2 diabetes patients display inflammation, elevated levels of cytokines and macrophages. The master regulator of inflammation in the islets is free fatty acids (FFA). It has already been reported that FFA and TLR4 stimulation induces pro-inflammatory factors in the islets. In this report we demonstrate that excess lipid triggers Fetuin-A (FetA) secretion from the pancreatic β-cells. Palmitate treatment to MIN6 cells showed significantly elevated FetA levels in respect to their controls. Fatty acid induces the FetA gene and protein expression in the pancreatic β-cells via TLR4 and over-expression of NF-κB. In the NF-κB knocked down MIN6 cells palmitate could not trigger FetA release into the incubation medium. These results suggest that NF-κB mediates palmitate stimulated FetA secretion from the pancreatic β-cells. Blocking the activity of TLR4 by CLI-095 incubation or TLR4 siRNA restored insulin secretion which confirmed the role of TLR4 in FFA-FetA mediated pancreatic β-cell dysfunction. Palmitate mediated expression of NF-κB enahnced inflammatory response through expression of cytokines such as IL-1β and IL-6. These results suggest that FFA mediated FetA secretion from pancreatic β-cells lead to their dysfunction via FFA-TLR4 pathway. FetA thus creates an inflammatory environment in the pancreatic islets that can become a possible cause behind pancreatic β-cell dysfunction in chronic hyperlipidemic condition. [ABSTRACT FROM AUTHOR]

Insulin resistance (IR) is an important determinant of type-2 diabetes mellitus (T2DM). Free fatty acids (FFAs) induce IR by various mechanisms. A surfeit of circulating FFA leads to intra-myocellular lipid accumulation that induces mitochondrial ROS generation and worsens IR. However, the molecular mechanisms behind are unclear. We identified thioredoxin interacting protein (TxNIP), which is overexpressed in T2DM, to be a promoter of ROS-induced IR. We observed upregulation of TxNIP upon palmitate treatment in skeletal muscle cells that led to ROS generation and Glut-4 downregulation resulting in impaired glucose-uptake. FFA-induced overexpression of TxNIP gene was mediated through the activation of its bona-fide trans activator, ChREBP. Further, Palmitate-induced impairment in AMPK-SIRT-1 pathway resulted in overexpression of ChREBP. While Fenofibrate, abrogated PA-induced TxNIP expression and ROS generation in skeletal muscle cells, Saroglitazar, a dual PPARα/γ-agonist, not only inhibited PA-induced TXNIP expression but also led to greater improvement in glucose uptake. Taken together, TxNIP appears to be an important factor in FFA-induced ROS generation and IR in skeletal muscle cells, which can be modulated for the management of this complex disorder. [ABSTRACT FROM AUTHOR]

Abstract: Aim: Asian Indians are believed to have a lower capacity to clear a glucose load even during normoglycemia. High post meal glucose levels have been linked to postprandial dyslipidemia and generation of proinflammatory cytokines. Since humans spend most of their time in the postprandial state, the present study aims to evaluate the relationship of insulin resistance (IR) in the basal state with dyslipidemia and systemic inflammation (hs-CRP, IL-6 and TNF-a), in the fasting state, 2h and 4h after a mixed meal, in Indian adults with normal glucose tolerance, and new onset type-2 diabetes. Methods: Forty-eight people with type 2 diabetes and 32 individuals with normoglycemia, 30–70 years age, not on medications, underwent blood sampling after overnight (12h) fast and 2 and 4h after a mixed meal (carbohydrates, proteins and fat content 79.1%, 7.7% and 13.2%, respectively). Results: Triglyceride (TG), TG/HDL-C (high density lipoprotein), HDL-C/LDL-C (low density lipoprotein) ratios, IR parameters, and inflammatory markers were significantly higher among patients with diabetes. There was a fall in total cholesterol (TC), HDL-C and LDL-C at 2 and 4h after the meal in both groups. Compared with fasting, 4-h postprandial TC, TG and HDL-C were significantly better positively correlated with IR in normal individuals. Postprandial hs-CRP was not significantly different to fasting in both groups. Postprandial IL-6 and TNF-α were significantly lower in both groups. Conclusion: Consumption of a carbohydrate rich meal is associated with a rise in TG and fall in TC, HDL-C, LDL-C, IL-6 and TNF-α among normal individuals and people with type 2 diabetes. [Copyright &y& Elsevier]

Abstract: Vitamin-D supplementation in vitamin-D insufficient/deficient prediabetes individuals is associated with significantly lower progression to diabetes (6/55 vs. 13/49; p =0.04) and higher reversal to normoglycemia (23/55 vs. 10/49; p =0.02), associated with decreased insulin resistance and systemic inflammation (TNFα and IL6). Baseline vitamin-D and 2h blood glucose independently predicted progression to diabetes. [Copyright &y& Elsevier]

Abstract: Prediabetes (IPD; n =122) and normoglycemic individuals (n =100) underwent assessment of polymorphisms of TNFα (−238, −308) and IL6 (−174). After 27.25±5.64 months, 16 IPD had reverted to normoglycemia and 18 progressed to diabetes. TNFα −238AA/GA genotypes were significantly more common in IPD, had higher TNFα, higher progression to diabetes and lower reversal. [Copyright &y& Elsevier]