Low-level inflammation of gut and obesity

In this journal, the research team discusses current knowledge about the mechanistic interactions between the gut microbiota, host energy metabolism, and the host immune system in the context of obesity and metabolic disease, with a focus on the importance of the axis that links gut microbes and host metabolic inflammation.

Because of the essential role of the gut ecosystem in maintaining host physiology, its alteration can trigger a wide range of physiological disorders, including chronic low-grade inflammation, metabolic disorders, excess lipid accumulation, and loss of insulin sensitivity, which increase the risk of developing metabolic diseases.

The researchers explore the complex mechanisms that link lipid metabolism, inflammation, insulin signaling, and obesity. They also discuss the influence of the gut microbiota in the onset of obesity and metabolic diseases through molecular interactions with energy metabolism and inflammation pathways of the host.

The gut microbiota can contribute to host insulin resistance, chronic low-grade inflammation, and fat deposition through a range of molecular interactions with the host and therefore can indirectly participate in the onset of obesity and metabolic diseases.

Obesity-related inflammation and impaired insulin action are tightly connected. Inflammation leads to impaired insulin action, which in turn contributes to the development of metabolic abnormalities. The emergence of chronic low-grade inflammation in individuals with obesity has been suggested to promote the clinical progression of the metabolic syndrome and obesity-related pathologies such as type-2 diabetes and non-alcoholic fatty liver disease.

Shifts in gut microbial composition caused by external factors can result in a dramatic alteration of the symbiotic relationship between gut bacteria and the host, which promotes the development of metabolic diseases. In particular, the gut microbiota is believed to contribute to metabolic diseases via stimulation of chronic low-grade inflammation.

It is important to note that although short chain fatty acids are a source of calories for the host, their intestinal production has been mostly associated with reduced inflammation and increased satiety (飽足) and with overall positive metabolic effects.

One of the hallmarks of obesity and obesity-related pathologies is the occurrence of chronic low-grade inflammation.

Lipopolysaccharides are derived from the outer cell membrane of Gram-negative bacteria, have been thought to initiate the inflammation-related processes associated with the onset of obesity and insulin resistance.

Low bacterial gene counts have also been associated with altered gut microbial functions and dysbiosis and have been linked to increased fat accumulation, lipopolysaccharide-induced inflammation, insulin resistance, obesity, and the metabolic syndrome.

Dysbiosis is a microbial imbalance or maladaptation on or inside the body, such as an impaired microbiota.

Randomized controlled studies have identified replacing markers of prebiotic treatment to be negatively correlated with weight gain, inflammation, and impaired glucose metabolism, which support the mechanisms observed in mammals.

Boulangé, C. L., (2016). Impact of the gut microbiota on inflammation, obesity, and metabolic disease. Biomedcentral. https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-016-0303-2?utm_campaign=BMCF_TrendMD_2019_GenomeMedicine&utm_source=TrendMD&utm_medium=cpc