Concepedia

Abstract

Background Myostatin (MSTN), a member of the transforming growth factor beta family, negatively regulates skeletal muscle mass. Deletion of the Mstn gene results in increased muscle mass. Also, Mstn-/mice and mice expressing a dominant negative MSTN receptor (activin receptor type IIB, ACVR2B) show decreased adipose tissue. Mstn-/mice fed a high fat diet gain less weight, have improved glucose tolerance and are more sensitive to insulin when compared to wild type controls. We are interested in characterizing molecules that may be downstream of MSTN signaling. We identified serotonin as a potential molecule that may interact with MSTN in skeletal muscle. Serotonin is thought to regulate both metabolism and cardiac hypertrophy, but it is not clear if serotonin is synthesized and functions in the skeletal muscle. We hypothesize that serotonin regulates skeletal muscle mass and metabolism, and the serotonin and myostatin pathways interact with each other.