Possible role of TUDCA bile acid in attenuating sarcopenia in senile mice

Abstract

The world health organization stipulates that by 2050 the population will have 2billion elderly people aged 60 and over, approximately 122% more than the current elderly population. With aging, the appearance of chronic diseases such as diabetes, cardiovascular diseases, among other sensory and bodily changes, such as the increase in white adipose tissue and loss of muscle mass, becomes more recurrent. Loss of muscle mass and/or strength, sarcopenia, is related to hormonal changes, insulin resistance, physical inactivity and lack of physical exercise, resulting from aging. The condition of sarcopenia makes the elderly more dependent and more likely to develop other diseases. For the treatment ofthese chronic diseases related to age, bile acids stand out, capable of regulating lipid, energy and glycemic metabolism. Among them, TUDCA is highly relevant, as it can improve insulin secretion and sensitivity, reduce body weight and blood glucose, inhibit cell death in hepatocytes and reduce the stress of the endoplasmic reticulum in several cell types. Little is known about the mechanisms triggered in muscle cells caused by the administration of this acid in the body. However, preliminary results from our group show that TUDCA can reduce adiposity and increase muscle mass in senile mice. We believe that these results may indicate modulations of compensation in the pathways of degradation and protein synthesis, possibly resulting in an improvement in sarcopenia. Therefore, with this project, we propose to investigate the role of bile acid TUDCA on the signaling of protein synthesis and degradation in the gastrocnemius and soleus muscles, as well as muscle glycogen stores, evaluating its potential in the treatment of sarcopenia in senile mice.