Orlistat augments postprandial increases in glucagon-like peptide 1 in obese type 2 diabetic patients

OBJECTIVE - Orlistat leads to improved glycemic control in obese type 2 diabetic patients, which is attributed to decreased insulin resistance associated with weight loss. Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are gut hormones that are secreted in response to food intake, and they both stimulate insulin secretion. Orlistat decreases fat absorption and increases intestinal fat content, which may lead to increased secretion of these peptides. In this pilot study, we tested the hypothesis that increased levels of these intestinal hormones may be involved in the improvement of postprandial hyperglycemia observed previously with orlistat in type 2 diabetic patients

Similar bacterial signatures in the gut microbiota of type 1 and type 2 diabetes patients and its association with G protein-coupled receptor 41 and 43 gene expression

Purpose There are conflicting reports regarding the abundance of short-chain fatty acids producing bacteria in the gut microbiota in patients with type 1 and type 2 diabetes. We aimed to determine the amount of Akkermansia muciniphila, Anaerobutyricum hallii, Bifidobacterium adolescentis, Bifidobacterium longum, Collinsella aerofaciens, Faecalibacterium prausnitzii, Lacticaseibacillus rhamnosus, and Parabacteroides distasonis in the gut microbiota in patients with type1 and type2 diabetes, compared with the healthy controls and analyze the correlation between the gene expression levels of two short-chain fatty acids receptors GPR41 and GPR43. Methods Forty type 1, 40 type 2 stool and blood samples of diabetes patients, and 40 healthy control samples were studied. DNA and RNA were extracted, and bacteria were detected using a Microbial DNA qPCR Assay kit. Gene expressions were detected with GPR41 and GPR43 primers via in-house qPCR. Results Compared with healthy controls, B.longum and F.prausnitzii abundance were significantly decreased in patients with type1 and type2 diabetes, A.hallii abundance was increased in patients with type1 and decreased in type2 diabetes contrarily A.muciniphila abundance was decreased in patients with type1 and increased in type2 diabetes. GPR43 gene expression was upregulated in both patients group, however GPR41 was upregulated only in patients with type2 diabetes. Conclusions Elevated B. longum and F. prausnitzii abundances were detected in the gut microbiota of patients with type1 and type2 diabetes and compared with healthy controls. B. longum and F.prausnitzii abundances were also correlated with the GPR43 gene expression level in type1 diabetes patients. Extensive studies determining bacteria producing short-chain fatty acids in gut microbiota, and their contribution in the pathogenesis of diabetes, are needed to understand better the mechanism of these diseases