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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
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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.
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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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