Steroid-induced diabetes: a clinical and molecular approach to understanding and treatment

Abstract

Since the advent of glucocorticoid therapy for autoimmune disease in the 1940s, their widespread application has led to the concurrent therapy-limiting discovery of many adverse metabolic side effects. Unanticipated hyperglycemia associated with the initiation of glucocorticoids often leads to preventable hospital admissions, prolonged hospital stays, increased risks for infection and reduced graft function in solid organ transplant recipients. Challenges in managing steroid-induced diabetes stem from wide fluctuations in post-prandial hyperglycemia and the lack of clearly defined treatment protocols. The mainstay of treatment is insulin therapy coincident with meals. This article aims to review the pathogenesis, risk factors, diagnosis and treatment principles unique to steroid-induced diabetes.

Keywords: glucocorticoids; insulin resistance; new onset diabetes after transplant; steroid-induced diabetes.

Conflict of interest statement

Conflict of interest: The authors have no conflicts of interest.

Copyright © 2013 John Wiley & Sons, Ltd.

Figures

Figure 1

The effect of glucocorticoids on glycerneogenesis in adipose tissue and liver. Phosphoenylpyruvate carboxykinase (PEPCK) is reciprocally upregulated in liver and downregulated in adipose by glucocorticoids. This results in a buildup of free fatty acids in the blood, which in turn result in insulin resistance and increase gluconeogenesis

Figure 2. Molecular basis of glucocorticoid (GC) action. See text for details. After van Raalte et al. [21]