Further evidence of altered adrenocortical function in hypertension. Dehydroepiandrosterone excretion rate

Nowaczynski, W.; Fragachán, F.; Silah, Jack G.; Millette, Bernard; Genest, Jacques

doi:10.1139/o68-155

Cited by 31 publications

(11 citation statements)

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“…Firstly, some epidemiologic studies report that serum DHEA and/or DHEA-sulfate levels in men are reduced in pathological states characterized by insulin resistance and hyperinsulinemia, such as obesity (55,56), hypertension (9,57), and untreated type II diabetes mellitus (58). The findings of this study suggest that enhancement of the MCRDHEA by insulin may contribute to the reduced serum DHEA levels observed in some of these pathologic conditions, at least as far as men are concerned.…”

Section: Discussionmentioning

confidence: 62%

Sex-specific action of insulin to acutely increase the metabolic clearance rate of dehydroepiandrosterone in humans.

Nestler

Kahwash²

1994

J. Clin. Invest.

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To test the hypothesis that insulin acutely enhances the metabolic clearance rate (MCR) of dehydroepiandrosterone in humans, the effect of a short-term insulin infusion on the MCR of dehydroepiandrosterone was assessed in 10 men and 7 women. After an overnight fast, dehydroepiandrosterone was infused at 3.47 jumol/h for 6.5 h. At 240 min, a hyperinsulinemic-euglycemic clamp was begun by infusing insulin at 21.5 pmol/kg per min for 2.5 h. MCR of dehydroepiandrosterone was calculated at baseline (210-240 min) and during the insulin infusion (360-390 min). A control study was conducted at least 1 wk later, in which 0.45% saline was substituted for the hyperinsulinemic-euglycemic clamp. During the insulin clamp study, serum insulin rose from 34±2 to 1084±136 pmol/liter (P = 0.0001) in men and from 40±5 to 1357+175 pmol/liter (P = 0.0003) in women, while serum glucose remained constant in both groups. MCR of dehydroepiandrosterone rose in men during the insulin infusion from 2443±409 to 3599±500 liters/ 24 h (P = 0.003), but did not change during the control saline infusion. In contrast, MCR of dehydroepiandrosterone in women did not change in the insulin clamp study during insulin infusion (2526±495 liters/24 h at baseline vs. 2442±491 liters/24 h during insulin infusion; P = 0.78). These findings suggest that insulin acutely increases the MCR of dehydroepiandrosterone in men but not in women.

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Section: Discussionmentioning

confidence: 62%

Sex-specific action of insulin to acutely increase the metabolic clearance rate of dehydroepiandrosterone in humans.

Nestler

Kahwash²

1994

J. Clin. Invest.

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“…However, this discrepancy seems not to exist in obesity only, since it was also present in patients with essential hypertension, as shown by Nowaczynski et al (28,29) and Dey et nl. (30).…”

Section: Dehydroepiandrostero Pzementioning

confidence: 85%

Dehydroepiandrosterone and Dehydroepiandrosterone Sulfate Dynamics in Obesity

Fehér¹,

Halmy²

1975

Can. J. Biochem.

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Dehydroepiandrosterone (D) and dehydroepiandrosterone sulfate (DS) dynamics were studied in three obese female subjects following a single injection of [4-14-CA1D and [7 alpha-3-H]-DS tracers. Dynamic parameters were calculated simultaneously by both the urinary and blood method of compartmentalization; Estimates for the urinary secretion and production rates of D were found to be high, and those of DS varied within normal range. Calculation of the conversion factors, rho DDS and rho DSD, by the urinary method revealed a noraml extraglandular DS yields D conversion, while that for D yields DS appeared deficient in obese female subjects. Estimates of inner and outer pool distribution volumes were extremely increased for free D; in contrast to this, moderately increased inner and decreased outer pool volumes of DS were observed. The metabolic clearance rates of D were normal or decreased and those for DS were greater than normal. The blood production rates of both B and DS were higher in obese female subjects than those estimated for normal women in our previous study; These observations suggest a considerable uptake of unconjugated D by adipose tissue, an overall poor D yields DS conversion and an accelerated DS metabolism in obese female subjects.

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“…Low plasma levels of these steroids in humans have been associated with the presence of cancer and may be related to increased risk ofdeveloping some types of cancer (14,15). Furthermore, low plasma levels of DHEAS are predictive of increased risk ofcardiovascular mortality in men (10), and are associated with some known risk factors for cardiovascular disease' including hypertension ( 16), and elevated serum lipids (17)(18)(19). DHEA has been reported to lower serum cholesterol in animals and to cause subjective improvement of intermittent claudication in humans (20,21).…”

mentioning

confidence: 99%

Reduction of atherosclerosis by administration of dehydroepiandrosterone. A study in the hypercholesterolemic New Zealand white rabbit with aortic intimal injury.

Gordon¹,

Bush²,

Weisman

1988

J. Clin. Invest.

220

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Dehydroepiandrosterone (DHEA) is an endogenous steroid that blocks carcinogenesis, retards aging, and exerts antiproliferative properties. In vitro, it is a potent inhibitor of glucose-6-phosphate dehydrogenase, the first committed step of the pentose phosphate pathway. In man, serum levels of DHEA and its sulfate peak in early adulthood and drop markedly with age. Epidemiologic evidence indicates that low levels of DHEA or its sulfate conjugate are linked to an increased risk of developing cancer or of death from cardiovascular disease. Like cancer, atherosclerosis is a proliferative process characterized by both initiation and promotion phases. This similarity provided a framework in which to study the antiatherogenic effects of DHEA.Rabbits were randomly assigned to four groups. Two groups of rabbits received aortic endothelial injury by balloon catheter and were fed a 2% cholesterol diet for 12 wk. DHEA, 0.5%, was incorporated into the diet of one group receiving the 2% cholesterol diet and endothelial injury and also into the diet of one of the control groups. Animals were killed after 12 wk and aortas, hearts, and livers were studied. Plasma samples were analyzed for total cholesterol, VLDL, LDL, HDL, triglycerides, DHEA, and DHEA-sulfate levels.The atherogenic insult resulted in severe atherosclerosis in animals not treated with DHEA. In those receiving DHEA there was an almost 50% reduction in plaque size (P = 0.006), inversely related to the serum level of DHEA attained. Fatty infiltration of the heart and liver were also markedly reduced. These beneficial actions were not attributable to differences in body weight gain, food intake, total plasma cholesterol or distribution of cholesterol among the VLDL, LDL, or HDL fractions.The results show that high levels of plasma DHEA inhibit the development of atherosclerosis and they provide an important experimental link to the epidemiologic studies correlating low DHEA-sulfate plasma levels with an enhanced risk of cardiovascular mortality.

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Further evidence of altered adrenocortical function in hypertension. Dehydroepiandrosterone excretion rate

Cited by 31 publications

References 0 publications

Sex-specific action of insulin to acutely increase the metabolic clearance rate of dehydroepiandrosterone in humans.

Sex-specific action of insulin to acutely increase the metabolic clearance rate of dehydroepiandrosterone in humans.

Dehydroepiandrosterone and Dehydroepiandrosterone Sulfate Dynamics in Obesity

Reduction of atherosclerosis by administration of dehydroepiandrosterone. A study in the hypercholesterolemic New Zealand white rabbit with aortic intimal injury.

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