Obesity And Gut Microbiota: A Comprehensive Review

Obesity is the multifactorial metabolic disease with worldwide interest, which leads to high non-communicable disease burden like type 2 diabetes, cardiovascular disease, and metabolic syndrome. Over the recent years, gut microbiota has been revealed as a master regulator of obesity pathogenesis. The imbalance of the composition of microbes in the gut or dysbiosis has been linked to higher energy harvest, lower energy expenditure, a change in lipid metabolism, and failing to control the appetite. Remarkably, a higher Firmicutes to Bacteroidetes ratio among the obese is a common behavior, which improves fermentation of the indigestible polysaccharides and leads to the production of short-chain fatty acids (SCFA) to facilitate adipogenesis. In addition, metabolites produced in the gut, including SCFAs, have context-specific effects on the metabolism of the host, and current evidence demonstrates that SCFAs exert both positive and negative effects on the rate of lipogenesis and inflammation. Neuroendocrine signaling by microbial metabolites regulating the gut-brain axis mediates the role of appetite and energy homeostasis. Moreover, Gram-negative bacterial endotoxin, lipopolysaccharides (LPS), causes metabolic endotoxemia and low-grade systemic inflammation to enhance insulin resistance and accumulation of lipids. Taken together, these mechanisms emphasise the imperative role of gut microbiota in development of obesity. Knowledge of the intricate host microbiota interactions may have therapeutic potentials, such as microbiota-specific treatments, namely probiotics, prebiotics, dietary manipulations, and fecal microbiota transplantation to treat the treatment of obesity.