The role of BCAA metabolism in metabolic health and disease

It has long been postulated that dietary restriction is beneficial for ensuring longevity and extending the health span of mammals, including humans. In particular, a reduction in protein consumption has been shown to be specifically linked to the beneficial effect of dietary restriction on metabolic disorders, presumably by reducing the activity of the mechanistic target of rapamycin complex (mTORC) 1 and the reciprocal activation of AMP-activated protein kinase (AMPK) and sirtuin pathways. Although it is widely used as a dietary supplement to delay the aging process in humans, recent evidence suggests that branched-chain amino acids (BCAAs) might be a major cause of the deteriorating effect of a protein diet on aging and related disorders. In this review, we delineate the regulation of metabolic pathways for BCAAs at the tissue-specific level and summarize recent findings regarding the role of BCAAs in the control of metabolic health and disease in mammals. This review article illustrates the function of branched-chain amino acids (BCAAs - essential nutrients we get from food) and how they’re processed in our bodies, in relation to health and illness. BCAAs are connected to aging processes and metabolic health - the body’s way of converting food into energy. Recent studies found that reducing BCAA intake can improve the health and lifespan of rodents. Similar studies were also conducted by using different animal models, like yeast, flies, rodents, and primates. It also emphasized the potential influence of BCAAs on human disease and aging metabolic processes. The review article concluded that BCAAs and their processing are vital for metabolic health and lifespan, and more research is needed to understand their effect on human health. Further studies on BCAAs could be important for creating diet plans and treatments for metabolic issues and aging-related diseases. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.