Diabetes and DHEA

A drop in DHEA-S levels is associated with the development of type 2 diabetes.

DHEA appears to increase insulin sensitivity. Insulin resistance is an early indicator of type 2 diabetes and closely associated with obesity, which are two of the major risks for heart disease.

Among women with impaired adrenal glands, taking DHEA has been shown to significantly increase insulin sensitivity. DHEA may therefore be a valuable treatment for type 2 diabetes. DHEA has also been shown to increase this sensitivity in obese women.

Clinical studies

  • In a 1993 study of a 15-year-old girl with type 2 diabetes, Professor C. Buffington reported that a dose of 150 mg of DHEA twice a day led to a marked improvement in sensitivity to insulin as indicated by a 30% improvement in the level of oral insulin tolerance, a three-fold greater rate of glucose synthesis, and a 30% increase in the binding of glucose to insulin. DHEA has therefore made it possible to increase sensitivity to insulin and therefore to improve the diabetic state.

  • Studies conducted by the Department of Experimental Medicine and Oncology, Section of General Pathology, University of Turin in Italy, show that oxidative stress plays a crucial role in the pathogenesis of chronic diabetic complications. Normoglycemic rats rendered diabetic by streptozotocin were treated with DHEA (4 mg/day) for 3 weeks. At the end of treatment, levels of hydroxynonenal, hydroperoxyeicosatetraenoic acid, antioxidants, as well as Na/K-ATPase activity and fatty acid membrane composition were assessed in kidney homogenates. Chronic hyperglycemia resulted in a marked increase in hydroxynonenal and lipoxygenase by-products and a decrease in both glutathione level and membrane Na/K-ATPase activity.
    DHEA treatment restored antioxidant levels to normal levels and significantly reduced hydroxynonenal and hydroperoxyeicosatetraenoic acid levels. In addition, DHEA compensated for the negative effect of hyperglycemia on membrane function: the decline in Na/K-ATPase activity in diabetic animals was strongly inhibited by DHEA treatment. These results show that DHEA reduces oxidative stress and the increase in residues produced by lipoxygenase induced by diabetes in the kidney of experimental rats. They also suggest that, by reducing the inflammatory response to oxidative stress, DHEA treatment may delay the progression of diabetic nephropathy.