The metabolic links between diet-induced changes in the gut and NASH iScience_CP MonashUni BakerResearchAu metabolic metabolism gut liver disease
By Dr. Priyom Bose, Ph.D.Jan 4 2023Reviewed by Danielle Ellis, B.Sc. Excessive intake of sucrose is a major driver of obesity and other diseases, such as non-alcoholic fatty liver diseases and the more severe non-alcoholic steatohepatitis . In addition, a high-caloric diet induces gut dysbiosis and inflammation, which in turn causes NASH. Recently, scientists reviewed the metabolic association between diet-induced alterations in the gut and NASH. This review is available in iScience.
Proteins are first converted into peptides and finally to amino acids. These are transported to the liver via the portal vein. In the liver, the toxic ammonia is quickly transformed into urea, which is eliminated from the body through urine. Obesity is related to increased body mass index , which has been linked with an increased mortality rate in both males and females. Diet-induced obesity increases the risk of incidence of many chronic conditions, such as cardiovascular diseases , type 2 diabetes mellitus , and several types of cancers . DIO enhances the accumulation of lipid droplets in the liver parenchyma, promoting NAFLD development.
The effects of macronutrients on the gut microbiota Gut microbiota plays an important role in gut energy metabolism. A high sugar and fatty food intake get rapidly absorbed in the small intestine, and a very small amount reaches the colon. As a result, the gut microbes are deprived of essential nutrients for their growth and survival. This finding reveals that consuming a high calorific and sugar diet leads to gut dysbiosis.
The downregulation of TJPs by HFrD leads to gut barrier deterioration, which promotes leakage of bacterial products and gut-derived metabolites into the portal circulation. This leakage causes LPS to reach the liver. In the liver, LPS binds to Toll-like receptor 4 on the macrophages and induces the release of inflammatory mediators, causing liver inflammation and the development of NAFLD/NASH.
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