Effects of gut microbiota on obesity and atherosclerosis via modulation of inflammation and lipid metabolism.

Recent studies have revealed a close relationship between inflammatory and metabolic pathways, and inflammation is now recognized to have a major role in obesity and metabolic diseases such as insulin resistance and atherosclerosis. The human body is home to a large number of distinct microbial communities, with the densest population in the distal gut (the gut microbiota). Bacteria have long been known to activate inflammatory pathways, and recent data demonstrate that the gut microbiota may affect lipid metabolism and function as an environmental factor that influences the development of obesity and related diseases. Here, we review how the gut microbiota may affect metabolic diseases by activating the innate immune system.

Caesar R ，Fåk F ，Bäckhed F 《-》

Effects of the gut microbiota on obesity and glucose homeostasis.

The human gut is home to a vast number of bacteria, the microbiota, whose genomes complement our own set of genes. The gut microbiota functions at the intersection between host genotype and diet to modulate host physiology and metabolism, and recent data have revealed that the gut microbiota can affect obesity. The gut microbiota contributes to host metabolism by several mechanisms including increased energy harvest from the diet, modulation of lipid metabolism, altered endocrine function, and increased inflammatory tone. The gut microbiota could thus be considered to be an environmental factor that modulates obesity and other metabolic diseases.

Greiner T ，Bäckhed F 《-》

Obesity, metabolic syndrome, and microbiota: multiple interactions.

Tilg H 《-》

Innate sensors of pathogen and stress: linking inflammation to obesity.

Pathogen and nutrient response pathways are evolutionarily conserved and highly integrated to regulate metabolic and immune homeostasis. Excessive nutrients can be sensed by innate pattern recognition receptors as danger signals either directly or through production of endogenous ligands or modulation of intestinal microbiota. This triggers the activation of downstream inflammatory cascades involving nuclear factor κB and mitogen-activated protein kinase and ultimately induces the production of inflammatory cytokines and immune cell infiltration in various metabolic tissues. The chronic low-grade inflammation in the brain, islet, liver, muscle, and adipose tissue further promotes insulin resistance, energy imbalance, and impaired glucose/lipid metabolism, contributing to the metabolic complications of obesity, such as diabetes and atherosclerosis. In addition, innate pathogen receptors have now emerged as a critical link between the intestinal microbiota and host metabolism. In this review we summarize recent studies demonstrating the important roles of innate pathogen receptors, including Toll-like receptors, nucleotide oligomerization domain containing proteins, and inflammasomes in mediating the inflammatory response to metabolic stress in different tissues and highlight the interaction of innate pattern recognition receptors, gut microbiota, and nutrients during the development of obesity and related metabolic disorders.

Jin C ，Flavell RA 《-》

Gut microbiota, intestinal permeability, obesity-induced inflammation, and liver injury.

Frazier TH ，DiBaise JK ，McClain CJ 《-》