Gut microbiota: a new path to treat obesity

Abstract

Obesity is a multifactorial disease resulting in excessive accumulation of adipose tissue. Over the last decade, growing evidence has identified the gut microbiota as a potential factor in the pathophysiology of both obesity and the related metabolic disorders. The gut microbiota is known to protect gastrointestinal mucosa permeability and to regulate the fermentation and absorption of dietary polysaccharides, perhaps explaining its importance in the regulation of fat accumulation and the resultant obesity. The proposed mechanisms by which the gut microbiota could contribute to the pathogenesis of obesity and the related metabolic diseases include: (a) a high abundance of bacteria that ferment carbohydrates, leading to increased rates of short-chain fatty acid (SCFA) biosynthesis, providing an extra source of energy for the host, that is eventually stored as lipids or glucose; (b) increased intestinal permeability to bacterial lipopolysaccharides (LPS), resulting in elevated systemic LPS levels that aggravate low-grade inflammation and insulin resistance; (c) increased activity of the gut endocannabinoid system. Fecal transplantation studies in germ-free mice have provided crucial insights into the potential causative role of the gut microbiota in the development of obesity and obesity-related disorders. Diet +/− bariatric surgery have been reported to modulate the gut microbiota, leading to lean host phenotype body composition. This review aims to report clinical evidence for a link of the gut microbiota with human obesity and obesity-related diseases, to provide molecular insights into these associations, and to address the effect of diet and bariatric surgery on the gut microbiota, including colonic microbiota, as a potential mechanism for promoting weight loss.

Bariatric Surgery in Obesity: Effects on Gut Microbiota and Micronutrient Status

“…Given the major anatomical and physiological changes of the GIT following BS, recently more attention has been focused on GM profile alteration following the surgical interventions. Along with diet, BS is a modulator of GM, promoting a lean host phenotype body composition [17].…”

High-Density Lipoproteins Are Bug Scavengers

“…In low-grade, chronic inflammation such as in periodontal disease and in obesity, whole-bacteria and/or bacterial components are transclocated from the oral environment or from the intestine into the blood flow, potentially triggering inflammation in distant tissues such as within the arterial wall or adipose tissue. Intestinal permeability is increased in obese patients, leading to LPS and peptogycane translocation and, potentially, even whole bacteria could reach the adipose tissue [137,138]. In periodontal disease, 16S bacterial DNA has been found in atherosclerotic tissue such as in carotid or aneurysmal samples [133,134].…”

Anti-inflammatory effect of piperine ameliorates insulin resistance in monosodium glutamate–treated obese mice

“…LPS is a strong stimulation to trigger the several cytokines associated with systemic insulin resistance [37]. Studies indicate that long-term high-calorie diets changed the composition of the intestinal microbiota of the body and showed that the number of Gram-negative bacteria increased and the amount of LPS secreted by it also increased, so the plasma LPS levels in obese patients are significantly higher than normal people [38,39]. LPS bind to complex of mCD14 and TLR-4 at the surface of the innate immune cells activate inflammatory pathway, and then triggers the secretion of pro-inflammatory cytokines consequently impact insulin action [40].…”