Toll Like Receptor 4: A Potential Link Between Obesity and Metabolic Diseases.

Abstract

Epidemiological evidence shows that obesity increases the risk of developing metabolic diseases. Nevertheless, the mechanisms behind this connection remain underappreciated. The substantial impact of these disorders on global health has led to extensive research efforts aimed at identifying the pathophysiological links between them. Chronic low-grade inflammation, induced by altered secretion of adipokines and other bioactive molecules, from adipose tissue, is believed to causally link obesity to various metabolic disorders. Multiple studies have indicated that TLR4 regulates inflammation, adipogenesis, thermogenesis, and glucose metabolism through its interaction with endotoxins, particularly in the context of obesity. The increased expression of TLR4 observed in obesity is believed to contribute to the development of type 2 diabetes (T2D), as it disrupts key physiological processes that regulate metabolic inflammation. This review aims to summarize recent research on the pathobiological roles of TLR4-mediated inflammation in obesity and its contribution to the development of metabolic disorders. Overall, current evidence supports a central role for TLR4 as a mediator of obesity-associated metabolic inflammation, highlighting TLR4 and its downstream pathways as promising targets for preventing or treating obesity related metabolic diseases.