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The effect of Lactobacillus plantarum- fermentation on the anti-diabetic functionality of Momordica charantia was examined using a high-fat-diet and low-dose streptozocin-induced type 2 diabetic rat model. Fermented Momordica charantia juice (FMCJ) administration mitigated the hyperglycemia, hyperinsulinemia, hyperlipidemia, and oxidative stress in diabetic rats more favorably than the non-fermented counterpart. Treatments with FMCJ improved ergosterols and lysomonomethyl-phosphatidylethanolamines metabolisms more effectively. Supplement of FMCJ regulated the composition of the gut microbiota, such as increased the abundance of Bacteroides caecigallinarum , Oscillibacter ruminantium, Bacteroides thetaiotaomicron, Prevotella loescheii , Prevotella oralis , and Prevotella melaninogenica , in diabetic rats compared with untreated diabetic rats. Moreover, FMCJ-treated diabetic rats exhibited higher concentrations of acetic acid, propionic acid, butyric acid, total short-chain fatty acids and lower pH values in colonic contents than that in non-fermented juice-treated rats. These results demonstrated that Lactobacillus plantarum -fermentation enhanced the anti-diabetic property of MC juice by favoring the regulation of gut microbiota and the production of SCFAs. Unlabelled Image • Fermentation improved serum glucose, insulin, and lipids in MCJ-treated diabetes. • Fermentation enhanced the regulatory effect of MCJ on lipid metabolism in diabetes. • Fermentation regulated the composition of gut microbiota in MCJ-treated diabetes. • Fermentation elevated colonic SCFAs contents in MCJ-treated diabetes. [ABSTRACT FROM AUTHOR]

Highlights • Fermentation affected the monosaccharide composition, Mw, and viscosity of MCP. • Fermentation improved serum glucose, insulin, and lipids in MCP-treated diabetes. • Fermentation enhanced the regulatory effect of MCP on oxidative stress in diabetes. • Fermentation improved the composition of gut microbiota in MCP-treated diabetes. • Fermentation increased colonic SCFAs in MCP-treated diabetic rats. Abstract The influence of Lactobacillus plantarum -fermentation on the structure and anti-diabetic effects of Momordica charantia polysaccharides were evaluated. High-fat diet and streptozotocin-induced type 2 diabetic rats were administrated with polysaccharides from fermented and non-fermented Momordica charantia (FP and NFP) for 4 weeks. Fermentation affected the physicochemical characterization, monosaccharide composition, molecular weight, and viscosity of Momordica charantia polysaccharides. Treatment with FP significantly ameliorated hyperglycemia, hyperinsulinemia, hyperlipidemia, and oxidative stress in diabetic rats compared with NFP. Moreover, the diversity and abundance of gut microbiota (Lactococcus laudensis and Prevotella loescheii) in diabetic rats were notably increased by treatment with FP in comparison to NFP. Meanwhile, FP-treated diabetic rats exhibited more colonic short-chain fatty acids (SCFAs) and lower pH values than that in NFP-treated rats. Overall, Lactobacillus plantarum- fermentation could enhance the anti-diabetes effects of Momordica charantia polysaccharides in rats by modifying the structure of polysaccharides to optimize gut microbiota and heighten the production of SCFAs. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM), a metabolic disease becoming ever more common, is the result of disturbed glyco- and lipid metabolism. On the basis of their inhibitory effects against several key enzymes linked to T2DM, synthetic antidiabetic agents have been developed and used for diabetic therapy, some with adverse side effects. Fortunately, many plant non-starch polysaccharides (NSPs) have been shown to possess inhibitory effects on the same T2DM-related enzymes. Through a simple literature search we found that α-amylase, α-glucosidase, lipase, and dipeptidyl-peptidase IV are the enzymes most often reported in the context of T2DM. In this short review we discuss published evidence for inhibition of these enzymes and the implications for treating T2DM. [ABSTRACT FROM AUTHOR]

Abstract Type 2 diabetes is a complex metabolic and endocrine disorder worldwide, which causes severe health and economic problems. The effects of polysaccharide from Plantago asiatica L. (PLP) on high-fat diet and streptozotocin-induced type 2 diabetic rats were examined. Administration of PLP caused significant decreases in the concentrations of blood glucose, insulin, total cholesterol, triglyceride, non-esterified fatty acid and maleic dialdehyde, and significant increases in the levels of high density lipoprotein-cholesterol and the activities of antioxidant enzymes compared with diabetic rats after 4 weeks’ treatment. The concentrations of short-chain fatty acids (SCFA) were significantly higher in the feces of diabetic rats after treatment with PLP. Moreover, colon bacterial diversity and abundance of bacteria, including Bacteroides vulgatus, Lactobacillus fermentum , Prevotella loescheii and Bacteroides vulgates were significantly increased by PLP treatment. These results indicated that the anti-diabetic effect of PLP in type 2 diabetic rats may be associated with regulation of gut microbiota and increased levels of SCFA. Graphical abstract Image Highlights • PLP attenuated hyperglycemia and hyperlipidemia in Type 2 diabetic rats. • PLP administration suppressed oxidative stress in Type 2 diabetic rats. • SCFA was significantly increased after PLP intake in Type 2 diabetic rats. • PLP improved structure of colon microbiota in Type 2 diabetic rats. [ABSTRACT FROM AUTHOR]

Objective: We evaluated whether the increasing number of genetic loci for coronary artery disease (CAD) identified in the general population could be used to predict the risk of major CAD events (MCE) among participants with type 2 diabetes at high cardiovascular risk.Research Design and Methods: A weighted genetic risk score (GRS) derived from 204 variants representative of all the 160 CAD loci identified in the general population as of December 2017 was calculated in 5,360 and 1,931 white participants in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) and Outcome Reduction With Initial Glargine Intervention (ORIGIN) studies, respectively. The association between GRS and MCE (combining fatal CAD events, nonfatal myocardial infarction, and unstable angina) was assessed by Cox proportional hazards regression.Results: The GRS was associated with MCE risk in both ACCORD and ORIGIN (hazard ratio [HR] per SD 1.27, 95% CI 1.18-1.37, P = 4 × 10-10, and HR per SD 1.35, 95% CI 1.16-1.58, P = 2 × 10-4, respectively). This association was independent from interventions tested in the trials and persisted, though attenuated, after adjustment for classic cardiovascular risk predictors. Adding the GRS to clinical predictors improved incident MCE risk classification (relative integrated discrimination improvement +8%, P = 7 × 10-4). The performance of this GRS was superior to that of GRS based on the smaller number of CAD loci available in previous years.Conclusions: When combined into a GRS, CAD loci identified in the general population are associated with CAD also in type 2 diabetes. This GRS provides a significant improvement in the ability to correctly predict future MCE, which may increase further with the discovery of new CAD loci. [ABSTRACT FROM AUTHOR]

Metformin is the first-line treatment for type 2 diabetes (T2D). Although widely prescribed, the glucose-lowering mechanism for metformin is incompletely understood. Here, we used a genome-wide association approach in a diverse group of individuals with T2D from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) clinical trial to identify common and rare variants associated with HbA1c response to metformin treatment and followed up these findings in four replication cohorts. Common variants in PRPF31 and CPA6 were associated with worse and better metformin response, respectively (P < 5 × 10-6), and meta-analysis in independent cohorts displayed similar associations with metformin response (P = 1.2 × 10-8 and P = 0.005, respectively). Previous studies have shown that PRPF31(+/-) knockout mice have increased total body fat (P = 1.78 × 10-6) and increased fasted circulating glucose (P = 5.73 × 10-6). Furthermore, rare variants in STAT3 associated with worse metformin response (q <0.1). STAT3 is a ubiquitously expressed pleiotropic transcriptional activator that participates in the regulation of metabolism and feeding behavior. Here, we provide novel evidence for associations of common and rare variants in PRPF31, CPA6, and STAT3 with metformin response that may provide insight into mechanisms important for metformin efficacy in T2D. [ABSTRACT FROM AUTHOR]

Objective: To identify genetic determinants of increased cardiovascular mortality among subjects with type 2 diabetes who underwent intensive glycemic therapy in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial.Research Design and Methods: A total of 6.8 million common variants were analyzed for genome-wide association with cardiovascular mortality among 2,667 self-reported white subjects in the ACCORD intensive treatment arm. Significant loci were examined in the entire ACCORD white genetic dataset (n = 5,360) for their modulation of cardiovascular responses to glycemic treatment assignment and in a Joslin Clinic cohort (n = 422) for their interaction with long-term glycemic control on cardiovascular mortality.Results: Two loci, at 10q26 and 5q13, attained genome-wide significance as determinants of cardiovascular mortality in the ACCORD intensive arm (P = 9.8 × 10-9 and P = 2 × 10-8, respectively). A genetic risk score (GRS) defined by the two variants was a significant modulator of cardiovascular mortality response to treatment assignment in the entire ACCORD white genetic dataset. Participants with GRS = 0 experienced a fourfold reduction in cardiovascular mortality in response to intensive treatment (hazard ratio [HR] 0.24 [95% CI 0.07-0.86]), those with GRS = 1 experienced no difference (HR 0.92 [95% CI 0.54-1.56]), and those with GRS ≥2 experienced a threefold increase (HR 3.08 [95% CI 1.82-5.21]). The modulatory effect of the GRS on the association between glycemic control and cardiovascular mortality was confirmed in the Joslin cohort (P = 0.029).Conclusions: Two genetic variants predict the cardiovascular effects of intensive glycemic control in ACCORD. Further studies are warranted to determine whether these findings can be translated into new strategies to prevent cardiovascular complications of diabetes. [ABSTRACT FROM AUTHOR]