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To investigate the significance of thrombelastography (TEG) in patients who have lung adenocarcinoma in situ (LAIS) complicated with type 2 diabetes (T2D), 120 subjects were enrolled: 40 with LAIS, 40 with LAIS and T2D (LAIS + T2D), and 40 healthy controls (HCs). Correlation analysis was used to assess the relationships of TEG with indicators of T2D. The LAIS + T2D group had lower reaction time (R), rate of clot formation (K), estimated percentage of lysis (EPL), and lysis after 30 min (LY30), but higher maximum amplitude (MA), angle (α), and coagulation index (CI) than other group. Compared with the HC group, the LAIS group had lower R, K, EPL, and LY30, but higher MA, α, and CI. In LAIS + T2D group, R and LY30 had negatively correlations with fasting blood glucose (FBG) and triglycerides (TGs); α and MA had positive correlations with FBG and TG; K had negative correlations with FBG; EPL had negative correlations with FBG and low-density lipoprotein (LDL); and CI had positive correlations with FBG and LDL. TEG may be a useful indicator of blood coagulation dysfunction in these patients rather the healthy individuals. [ABSTRACT FROM AUTHOR]

Introduction: Diabetes mellitus (DM) is prevalent in developed and developing countries, including China. However, few studies have examined the potential risk factors for albuminuria in normotensive older adults with type 2 DM and normal renal function. Methods: We recruited normotensive older adults (≥ 65 years) with type 2 DM and normal renal function from the First Affiliated Hospital of Soochow University from January to December 2019. We stratified participants according to their urine albumin to creatinine ratio (ACR) into the following groups: normal ACR (ACR1), microalbuminuria (ACR2), and macroalbuminuria (ACR3). Demographic characteristics, anthropometric parameters, and metabolic profiles were recorded. Creatinine clearance (Ccr) and homeostasis model assessment—insulin resistance (HOMA-IR) were calculated. Logistic regression was used to examine risk factors for albuminuria. Results: A total of 250 older adults were enrolled during the study period, including 124, 82, and 44 with normal albuminuria, microalbuminuria, and macroalbuminuria, respectively. We found that an extended duration of DM (odds ratio [OR] 1.085, 95% confidence interval [CI] 1.012–1.164, P = 0.022), elevated systolic blood pressure (OR 1.049, 95%CI 1.018–1.081, P < 0.01), elevated glycated hemoglobin (OR 1.734, 95% CI 1.332–2.258, P < 0.01), low insulin (OR 0.871, 95% CI 0.804–0.944, P < 0.01), and low C-peptide (OR 0.365, 95% CI 0.239–0.588, P < 0.01) were independent risk factors for albuminuria. Conclusion: Elevated blood pressure, low insulin, low C-peptide, and poor glycemic control were significant risk factors for albuminuria. These parameters may serve as early indicators for intervention. [ABSTRACT FROM AUTHOR]

Aims. Obesity is highly associated with type 2 diabetes mellitus (T2DM). The TIM3/galectin-9 pathway plays an important role in immune tolerance. Herein, we aimed to investigate the expression of TIM3 and galectin-9 in peripheral blood and to evaluate their clinical significance in patients with obesity and obesity-related T2DM. Methods. We performed flow cytometry on peripheral blood samples from healthy donors (HC), patients with simple obesity (OB), and patients with obesity comorbid T2DM (OD). The expression of TIM3 on CD3+, CD4+, and CD8+ T cells was determined. The level of galectin-9 in plasma was detected by ELISA. Results. We demonstrated the enhancement of TIM3 on CD3+, CD4+, and CD8+ T cells in the OB group when compared with healthy controls, while it was decreased significantly in the OD group. The TIM3+CD8+ T cells of the OB group were positively correlated with risk factors including BMI, body fat rate, and hipline. The concentration of galectin-9 of the OD group in plasma was significantly higher than that of healthy donors and the OB group. Moreover, the level of galectin-9 of the OD group was positively correlated with fasting insulin and C-peptide, which were two clinical features that represented pancreatic islet function in T2DM. Conclusions. Our results suggested that TIM3 and galectin-9 may be potential biomarkers related to the pathogenesis of obesity-related T2DM. [ABSTRACT FROM AUTHOR]

Summary: A systematic review and meta‐analysis of observational studies was performed to provide a deeper understanding of the associations between foetal and childhood exposure to famine and the risks of type 2 diabetes mellitus (T2DM), metabolic syndrome, hypertension, hyperglycaemia, dyslipidaemia, obesity, overweight, coronary heart disease, stroke, and nonalcoholic fatty liver disease (NAFLD) in adulthood. Both foetal and childhood exposure to famine were positively associated with the risks of T2DM (foetal exposure: RR 1.37, 95% CI, 1.23‐1.52; childhood exposure: RR 1.33, 95% CI, 1.08‐1.64), metabolic syndrome (RR 1.26, 95% CI, 1.07‐1.50; RR 1.24, 95% CI, 1.13‐1.35), hypertension (RR 1.30, 95% CI, 1.07‐1.57; RR 1.33, 95% CI, 1.02‐1.74), hyperglycaemia (RR 1.27, 95% CI, 1.11‐1.45; RR 1.25, 95% CI, 1.10‐1.42), dyslipidaemia (RR 1.48, 95% CI, 1.33‐1.66; RR 1.27, 95% CI, 1.12‐1.45), obesity (RR 1.19, 95% CI, 1.02‐1.39; RR 1.13, 95% CI, 1.00‐1.28), overweight (RR 1.17, 95% CI, 1.07‐1.29; RR 1.07, 95% CI, 1.00‐1.14), coronary heart disease (RR 1.22, 95% CI, 1.00‐1.51; RR 1.21, 95% CI, 1.09‐1.35), and moderate‐to‐severe NAFLD (RR 1.66, 95% CI, 1.07‐2.57; RR 1.68, 95% CI, 1.41‐1.99) in adulthood. No association was observed for the risks of stroke or mild NAFLD. Adjustments for age, alcohol, smoking, body mass index, and physical activity nullified some associations. The associations were generally stronger in women than in men. In summary, foetal and childhood exposure to famine may confer greater risks of developing certain cardiometabolic conditions in adulthood, particularly in women. The extent to which risks for cardiometabolic conditions are associated with early‐life famine appears to be determined by certain factors in adulthood. [ABSTRACT FROM AUTHOR]

Summary: Certain glucose‐lowering medications have been implicated in the risk of fracture. While there is convincing evidence from randomized controlled trials (RCTs) that thiazolidinedione use is associated with a higher risk of fracture, the effects of metformin, insulin, and sulphonylureas on the risk of fracture remain equivocal because these medications are not generally investigated in RCTs. A meta‐analysis of observational studies to provide further insights into the association between the use of metformin, insulin, sulphonylureas, or thiazolidinediones and the risk of fracture was performed. PubMed and Web of Science databases were searched to identify relevant observational studies. A random effects model was used to estimate the summary relative risks (RRs) with 95% confidence intervals (CIs). The use of insulin (RR 1.49, 95% CI 1.29, 1.73; n = 23 studies), sulphonylureas (RR 1.30, 95% CI 1.18, 1.43; n = 10), and thiazolidinediones (RR 1.24, 95% CI 1.13, 1.35; n = 14) was associated with an increased risk of fracture, whereas the use of metformin was associated with a reduced risk of fracture (RR 0.86, 95% CI 0.75, 0.99; n = 12). Regarding types of thiazolidinediones, both pioglitazone (RR 1.38, 95% CI 1.23, 1.54; n = 5) and rosiglitazone (RR 1.34, 95% CI 1.14, 1.58; n = 5) were positively associated with the risk of fracture. In summary, there is compelling evidence to discourage the use of thiazolidinediones in individuals with an increased risk of fracture, whereas metformin appears to have a good safety profile for the risk of fracture. The reduced risk of fracture with metformin could possibly be due to the reduced overall risk of fracture among metformin users, as this medication is typically prescribed in the early stages of type 2 diabetes mellitus. The use of insulin or sulphonylureas may increase fracture risk; this risk is most likely attributed to an increased risk of hypoglycaemia‐induced falls. Further confirmation by additional RCTs is required to determine whether the observed association between the use of metformin, insulin, or sulphonylureas and the risk of fracture is due to treatment with these medications or confounding factors. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) and its causal factors of hepatic insulin resistance (IR) and type 2 diabetes are rapidly growing worldwide. Developing new therapeutic methods for these conditions requires a comprehensive understanding between hepatic lipid metabolism and IR. Sterol regulatory element-binding transcription factor 1c (SREBP-1c) and carbohydrate responsive-element binding protein (ChREBP) are the major regulators of fatty acid synthase (FASN), a key enzyme of de novo fatty acid synthesis. They are induced by insulin, which directly binds to the sterol regulatory elements (SRE) or carbohydrate-responsive elements (ChORE) of the FASN promoter to induce its expression. The insulin pathway involved in NAFLD has well studied, but the role of histone modification in NAFLD is just beginning to be investigated, and there is minimal data regarding its involvement. In the current study, we investigated histone modifications in FASN under insulin stimulation. H3K4 hypertrimethylation and H3, H4 hyperacetylation in the FASN promoter was found in HepG2 cells and primary hepatocytes following insulin stimulation. We also found that insulin treatment induced the transcription factor SREBP-1c, ChREBP and could accelerate FASN expression by enhancing SREBP-1c, SRE, and ChREBP ChORE binding and inducing H3, H4 hyperacetylation at SRE, ChORE, or transcription start site (TSS) regions of the FASN promoter in hepatocellular carcinoma cell line (HepG2) and primary hepatocytes. Finally, histone acetylation could influence FASN expression by impairing SREBP-1c SRE and ChREBP ChORE binding. [ABSTRACT FROM AUTHOR]

Globally, diabetes mellitus is not only considered a leading cause of mortality and morbidities but has also created a substantial economic burden. There is growing evidence that foods and their components can be implemented in the prevention and management of type 2 diabetes mellitus (T2DM). Increased dairy consumption has been linked to a lower risk of T2DM. The protective role of dairy foods in the development of T2DM is thought to be largely attributable to dairy nutrients, one of them being dairy protein. There is considerable evidence that milk proteins increase the postprandial insulin response and lower the postprandial blood glucose response in both healthy subjects and patients with T2DM. The exact mechanisms by which milk proteins lower postprandial glucose levels are yet to established; however, the amino acids and bioactive peptides derived from milk proteins are thought to modify a physiological milieu, which includes delayed gastric emptying and the enhancement of incretin and insulin responses, consequently leading to lower postprandial glucose levels. The present review will focus on providing a clear presentation of the potential implementation of milk proteins as a dietary supplement in the prevention and management of T2DM by summarizing the relevant supporting evidence for this particular topic. [ABSTRACT FROM AUTHOR]