gut microbes have a role in the host's metabolic homeostasis
lipopolysaccharide (LPS)
Associations between circulating LPS level, consumption of a high-fat diet and the presence of obesity and type 2 diabetes mellitus have been confirmed in humans
high-fat diet induces metabolic endotoxemia in healthy individuals.
A link between energy intake (high-fat diet) and metabolic endotoxemia has also been described
associations have been proposed between high-fat diet, metabolic endotoxemia and levels of inflammatory markers (TLRs and SOCS3) in mononuclear cells
metabolic endotoxemia is associated with systemic and adipose tissue inflammation in pregnant women with obesity
A growing amount of evidence indicates that changes in the integrity of the intestinal barrier occur both in the proximal and the distal part of the gut, which can contribute to the entrance of LPS into the systemic circulation
intestinal endocannabinoid system
The low-grade systemic inflammation that characterizes the obese phenotype is controlled by peptides that are produced in the gut. These peptides are influenced by the presence or absence of the gut microbiota
these findings suggest that the gut microbiota modulates the biological systems that regulate the availability of nutrients, energy storage, fat mass development and inflammation in the host, which are all components of the obese phenotype
good look of how the the gut health, or lack there of, can influence energy homeostasis and contribute to obesity. This article points to the presence of LPS playing a role in metabolic endotoxemia. It does discuss the importance of the microbiota and their possible role in the low-grade systemic inflammation condition that is obesity.
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