A Close Association between Insulin Resistance and Dehydroepiandrosterone Sulfate in Subjects with Essential Hypertension.

Abstract

Abstract.To examine the serum levels of dehydroepiandrosterone sulfate (DHEAS) and its relation with insulin resistance and the other risk factors in essential hypertension, serum DHEAS and insulin sensitivity were assessed in 35 male hypertensive and 17 male healthy control subjects aged 50-59 years. Fasting plasma insulin and the area under curve of plasma insulin were determined during a 75 g oral glucose tolerance test. Insulin sensitivity was measured by the steady state plasma glucose method. Fasting plasma insulin and the area under curve of plasma insulin were significantly higher in the hypetensive group than in control group. Steady state plasma glucose was significantly higher in hypertensive subjects indicating insulin resistance compared with control subjects.On the other hand, fasting serum DHEAS levels were significantly lower in the hypertensive group than in the control group. Fasting serum DHEAS levels were inversely correlated with steady state plasma glucose significantly (p=0.0008), indicating a close association between DHEAS levels and insulin resistance.Fasting serum DHEAS was inversely correlated with systolic blood pressure and fasting plasma insulin. In multiple regression analysis of hypertensive subjects, steady state plasma glucose was the strongest determinant of the fasting serum level of DHEAS, followed by systolic blood pressure and fasting plasma insulin. These 3 factors accounted for 51.6% of the variation in DHEAS.In nonobese and nondiabetic essential hypertension, serum DHEAS was lower and insulin resistance was the most significant independent determinant of reduced serum DHEAS, followed by systolic blood pressure and fasting plasma insulin. [7, 8] were found to be associated with insulin resistance. In non-diabetic men, decreased serum DHEAS levels were related to higher insulin concentrations, suggesting insulin resistance [9]. Nevertheless, no study has investigated direct relationship between DHEAS and insulin resistance measured by a precise method in hypertensive subjects.The purpose of this study was primarily to determine if serum DHEAS levels are changed in subjects with essential hypertension compared with healthy controls, and secondarily to evaluate the relationship

The Effect of Physiologic Hyperinsulinemia during an Oral Glucose Tolerance Test on the Levels of Dehydroepiandrosterone (DHEA) and Its Sulfate (DHEAS) in Healthy Young Adults Born with Low and with Normal Birth Weight

“…Zietz et al also observed lower DHEA/cortisol rates in type2 diabetic men compared to healthy people [21]. Suzuki et al found that insulin resistance is the most important independent determinant of low DHEAS levels [22]. To the contrary, studies suggesting the inducing effect of insulin on the production of adrenal androgens were carried out under physiological insulin levels.…”

The adrenal and the metabolic syndrome

“…In a second study from Japan, the relationship between DHEA-sulfate (DHEAS) and insulin resistance was examined in 35 hypertensive and 17 normotensive humans aged 50 to 59 years [18]. Insulin sensitivity was measured by the steady-state glucose method.…”

Metabolic effects of dehydroepiandrosterone replacement therapy in postmenopausal women

“…Observational studies in insulin-resistant conditions such as age (19), essential hypertension (20) and female hyperandrogenism (21) clearly demonstrate an association between low DHEA-S plasma concentrations and reduced insulin sensitivity. Intervention studies with DHEA supplementation, however, have given con¯icting results: improvement of insulin sensitivity in experimental animals (22); no modi®cation of insulin sensitivity in polycystic ovary syndrome (PCOS) with short-term infusion (23), in normal individuals undergoing shortterm administration (24), in obese adolescents (25) and adults (26) with medium-term treatment and in postmenopausal women after long-term substitution (27); amelioration of insulin resistance in a case of diabetes and hyperandrogenism (28).…”