Minireviews
Copyright ©The Author(s) 2015.
World J Diabetes. Jul 25, 2015; 6(8): 1073-1081
Published online Jul 25, 2015. doi: 10.4239/wjd.v6.i8.1073
Table 1 Pathophysiology of corticosteroid-induced hyperglycemia
Increase in insulin resistance with increased glucose production and inhibition of the production and secretion of insulin by pancreatic β-cells
Corticosteroids increase endogenous glucose production, increment in gluconeogenesis and antagonizing the metabolic actions of insulin
Enhance the effects of other counterregulatory hormones, such as glucagon and epinephrine, which increase the endogenous synthesis of glucose
Also been shown that the expression of the nuclear receptor peroxisome proliferator-activated receptor α is necessary for the increment in endogenous glucose production induced by corticosteroids
Corticosteroids reduce peripheral glucose uptake at the level of the muscle and adipose tissue
Costicosteroids also inhibit the production and secretion of insulin from pancreatic β-cells and induce β-cell failure indirectly by lipotoxicity