Purpose of review: Impairment of glucose metabolism is commonly encountered in Cushing's syndrome. It is the source of significant morbidity and mortality even after successful treatment of Cushing's. This review is to understand the recent advances in understanding the pathophysiology of diabetes mellitus from excess cortisol.
Recent findings: In-vitro studies have led to significant advancement in understanding the molecular effects of cortisol on glucose metabolism. Some of these findings have been translated with human data. There is marked reduction in insulin action and glucose disposal with a concomitant, insufficient increase in insulin secretion. Cortisol has a varied effect on adipose tissue, with increased lipolysis in subcutaneous adipose tissue in the extremities, and increased lipogenesis in visceral and subcutaneous truncal adipose tissue.
Summary: Cushing's syndrome results in marked impairment in insulin action and glucose disposal resulting in hyperglycemia. Further studies are required to understand the effect on incretin secretion and action, gastric emptying, and its varied effect on adipose tissue.