Human PYY ELISA Kit

Metabolic surgery is an effective therapy for diabetic patients with obesity. The main mechanisms underlying the effects of metabolic surgery include food intake restriction and the accompanying reduced daily caloric intake and changes in gut hormones and bile acid. Insulin resistance and impaired beta-cell function contribute to the development of type 2 diabetes. An increasing number of studies have focused on the central role of islet function in type 2 diabetes. In this article, we review the related high-quality literature and summarize the following mechanisms and principles underlying metabolic surgery in the context of islet function protection: (1) reduced glucotoxicity and chronic inflammation help facilitate better beta-cell function and the preservation of beta-cell mass following metabolic surgery; (2) based on the increased levels of GLP-1 and PYY after metabolic surgery, gut hormones appear to play a significant role in improving beta-cell function through the GLP-1R signaling pathways; (3) the bile acid signaling pathway could affect beta-cell function; and (4) the GLP-1R and bile acid signaling pathways could also cause other endocrine cells to contribute to islet function.

The intestinal epithelium is an active barrier separating the host from its microbiota. It senses microbial compounds through expression of a wide range of receptors including the Toll-like receptors (TLRs). TLRs have been shown to regulate epithelium permeability or secretion of defensin by Paneth cells. However, the expression and function of TLRs in enteroendocrine L-cells, a specific subtype of intestinal cells secreting PYY and GLP-1, have not yet been assessed. PYY and GLP-1 are implicated in regulation of gut motility, food intake and insulin secretion, and are of great interest regarding obesity and type 2 diabetes. Using a cellular model of human L-cells and a reporter system for NF-kappa B activation pathway, we reported functional expression of TLRs in these cells. Stimulation with specific TLR-agonists increased expression of Pyy but not Proglucagon in an NF-kappa B-dependent manner. Moreover, the effect of TLR stimulation was additive to butyrate, a product of bacterial fermentation, on Pyy expression. Additionally, butyrate also increased Tlr expression, including Tlr4, and the NF-kappa B response to TLR stimulation. Altogether, our results demonstrated a role of TLRs in the modulation of Pyy expression and the importance of butyrate, a product of bacterial fermentation in regulation of microbial TLR-dependent sensing.