Insulin resistance and sarcopenia

Abstract

If there is a disease directly associated with adiposity, it is type 2 diabetes mellitus (T2DM), whose pathophysiological framework has historically revolved around insulin resistance (IR), a phenomenon closely linked to increasing adiposity.
During my training at the National University of Colombia, academic discussions aimed at deciphering the pathophysiology of IR always seemed to approach an enigma. It was much later that I came to understand the role of adipocyte dysfunction and the ectopic migration of fatty acids into vital organs such as the pancreatic ?-cell, the hepatocyte, and, of course, skeletal muscle.
In 2001, during the highly anticipated Banting Lecture, Dr. McGarry (1) emphasized the importance of intramyocellular fat in the pathophysiology of IR and diabetes. It was then that I understood that if we were unable to combat obesity itself, we should at least attempt to minimize its impact on skeletal muscle.
This concept brings me to a decade later, in 2011, when Dr. Srikanthan (2) described an inverse relationship between IR—measured using the HOMA index (Homeostatic Model Assessment)—and skeletal muscle mass: each increase in muscle mass (MM) consistently leads to a reduction in IR, unmatched by any medication, not even metformin or thiazolidinediones. So, why not treat diabetes by increasing MM?