Anti-Peptide YY polyclonal antibody

Novel treatment methods for obesity are urgently needed due to the increasing global severity of the problem. Gastrointestinal hormones, such as GLP-1 and PYY, are secreted by the enteroendocrine cells, playing a critical role in regulating food intake. Digested nutrients trigger the secretion of these hormones, which have a very short half-life. alpha-Linolenic acid (alpha LA) has been shown to stimulate GLP-1 secretion, however, chemical instability and fast uptake in the small intestine hinder its use in body weight management. We developed a novel delivery system based on inorganic mesoporous particles for alpha LA to increase secretion of gastrointestinal peptides. alpha LA was loaded to thermally hydrocarbonized porous silicon particles (THCPSi). 47.9 +/- 3.84% and 30.7 +/- 2.86% of alpha LA was released during 6 h from 3.0% and 9.2% loading degree (w/w) samples in vitro, respectively. Native alpha LA (50 mu M) significantly increased GLP-1 secretion from enteroendocrine STC-1 and GLUTag cell lines. alpha LA loaded THCPSi significantly and dose dependently stimulated GLP-1 secretion from STC-1 cells, whereas empty particles did not. We demonstrated in vitro that THCPSi particles have the potential to be used as a controlled delivery system for nutrients such as alpha LA, increasing GLP-1 secretion. Our results justify further in vivo investigations.

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.