PURPOSE OF REVIEW

To summarize the epidemiology of myosteatosis and its association with diabetes.

RECENT FINDINGS

The role of myosteatosis (fat infiltration in skeletal muscle) in diabetes has received considerable attention. There is reasonably consistent evidence that myosteatosis contributes to glucose and insulin abnormalities and diabetes, possibly even independent of overall obesity. Novel hypotheses that link myosteatosis with insulin resistance and type 2 diabetes have also recently been proposed. These hypotheses suggest that impaired secretion of adipokines, modulation of nutritive blood flow to skeletal muscle, or both may be of importance for the development of myosteatosis. Recent longitudinal data also suggest that myosteatosis increases with aging, regardless of changes in body weight.

SUMMARY

Further studies are needed to identify the specific physiological mechanisms that influence myosteatosis, and the mechanisms that link this fat depot with insulin resistance. Longitudinal studies are also needed to evaluate the remodeling of skeletal muscle fat with aging, across a wider age spectrum, and across different populations, especially those at high risk of developing diabetes. There is also a need to evaluate whether myosteatosis influences the incidence of type 2 diabetes independent of overall adiposity. A better understanding of the factors that regulate myosteatosis may lead to the development of novel therapies that influence a more metabolically 'healthy' skeletal muscle.