Understanding the role of PRRs, SCFA, Adipose tissue markers and Liver Markers followed by Gut Microbiota Shift in High Sucrose Diet Induced Type 2 Diabetes

Abstract

Diabetes is the chronic metabolic syndrome in which glucose metabolism will be impaired, and caused by several factors such as ageing, stress, environment, food habits, etc. Obesity and insulin resistance are associated with low grade inflammation which progress in to type 2 diabetes mellitus (T2DM). The gut microbiota is now considered as one of the most important environmental factors impacting on host physiology and metabolism. Role of this ‘organ’ on the onset of insulin resistance and the low grade inflammatory tone characterizing obesity has been found recently. Obesity affects a large number of individuals worldwide; it degrades human health and quality of life. Gut microbiota plays role in the pathophysiology of obesity and type 2 diabetes, which is promoted by a bacterial diversity shift mediated by over nutrition. Whole bacteria, their products, and metabolites undergo increased translocation through the gut epithelium to the circulation due to degraded tight junctions and the consequent increase in intestinal permeability that results in inflammation and insulin resistance. Healthy mammalian gut is colonized by trillions of microbes, which lives in symbiotic relationship with host. High sugar diet influences the gut microbiota composition. Alteration in gut microbiome also influenced the pattern of specific metabolic capabilities of the host. The products of the gut microbiota like short-chain fatty acid (SCFA), vitamins and other metabolites are absorbed and reach to blood circulation, from blood it reaches to the tissue where because of these products, inflammation occurs and leads to production of pro inflammatory cytokines, which causes insulin resistance. In this study animal model of type 2 diabetes is connected with altered gut microbiota and alteration in energy harvest from the food. This study was designed to understand the effect of gut microflora alteration using gram-negative spectrum specific antibiotic on pathogenesis of high sucrose diet mediated type 2 diabetes. The effects of altering the microflora are estimated by studying the altered biochemical parameters, gene expression of pattern recognition receptors (PRRs), adipose tissue markers (Leptin, Adiponection, IL-6, TNF-α) and liver tissue markers (LXRs, RXRs) as well as metabolite's analysis of SCFAs. Through these, we are trying to understand possible molecular pathways induced by alteration in gut microbiota and their metabolites. ABSTRACT Nirma University In our work, we discuss putative mechanisms linking gut microbiota and T2D. These data underline the advantage of investigating and changing the gut microbiota as a therapeutic target in the context of obesity and T2D.