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Diabetes and DHEA


A decrease in DHEA-S 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 is closely associated with obesity, which are both major risk factors for heart disease.

Among women with deficient adrenal glands, DHEA supplementation was shown to significantly increase insulin sensitivity. DHEA might be a valuable treatment for type 2 diabetes. DHEA has also been shown to increase insulin sensitivity among obese women.


Clinical Studies

  • In a 1993 case report study of a 15 year old woman with Type II diabetes, C. Buffington and co-workers reported that a 150 mg twice daily dose of DHEA led to a marked improvement in insulin sensitivity, as determined by a more than 30 % reduction in fasting and oral glucose tolerance test insulin levels, a threefold stimulation of the rate of glucose disappearance with intravenous insulin, and a 30% increase in insulin binding. DHEA improved insulin sensitivity and ameliorated the diabetic state.

  • Department of Experimental Medicine and Oncology, General Pathology Section, University of Turin, Turin, Italy. Oxidative stress plays a crucial role in the pathogenesis of chronic diabetic complications. Normoglycemic and streptozotocin-diabetic rats were treated with dehydroepiandrosterone (DHEA) (4 mg/d per rat) for 3 weeks. At the end of treatment, hydroxynonenal, hydroperoxyeicosatetraenoic acids and antioxidant levels, as well as Na/K-ATPase activity and membrane fatty acids composition were evaluated in kidney homogenates. Chronic hyperglycemia caused a marked increase of both hydroxynonenal and lipoxygenase pathway products and a drop in both GSH levels and membrane Na/K-ATPase activity. DHEA treatment restored the antioxidant levels to close to the control value and considerably reduced hydroxynonenal and hydroperoxyeicosatetraenoic acid levels. Moreover, DHEA counteracted the detrimental effect of hyperglycemia on membrane function: the drop of Na/K-ATPase activity in diabetic animals was significantly inhibited by DHEA treatment. These results show that DHEA reduces oxidative stress and the consequent increase of lipoxygenase pathway products induced by experimental diabetes in rat kidney; they also suggest that, by reducing the inflammatory response to oxidative stress, DHEA treatment might delay the progression of diabetic kidney disease.










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