Such_Saturation
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Hyperglycaemia acutely decreases circulating dehydroepiandrosterone levels in healthy men. - PubMed - NCBI
Over the past two decades, an abundant literature has focused on the adrenal androgens dehydroepiandrosterone sulphate (DHEAS) and dehydroepiandrosterone (DHEA) and their relation with immunity, ageing, obesity, diabetes and cardiovascular diseases in humans. Low levels of DHEAS predict cardiovascular mortality in men. It is known that type 2 diabetes is associated with a two- to fourfold higher risk of coronary heart disease (CHD) and lower levels of DHEAS than nondiabetic men. Whether these low circulating adrenal androgen levels are a primary phenomenon that links type 2 diabetes and CHD is questioned. At least three, main confounding factors may interfere (i.e. high adiposity, hyperinsulinism and hyperglycaemia). Adrenal androgen levels tend to be lower in overweight subjects and are associated with visceral fat accumulation. Although most but not all studies showed no association between fasting insulin concentrations and DHEAS or DHEA levels, experimentally induced hyperinsulinaemia was associated with decreased DHEA and DHEAS levels in healthy men. In addition, the lowering of fasting insulinaemia observed during diet-induced weight loss was associated with increased DHEAS levels in obese men. These findings suggest that insulin variations might influence DHEA and DHEAS levels in men. On the other hand, blood glucose levels itself might influence DHEAS and DHEA concentrations. For example, a negative correlation between the area under the plasma glucose curve during oral glucose tolerance test (OGTT) and serum DHEAS and DHEA levels was observed in Japanese men with impaired glucose tolerance and in normal glucose-tolerant Caucasians. DHEAS was also found to be inversely related with 2-h glucose in nondiabetic men. However, these correlations disappeared when the analysis accounted for adiposity. Thus, it remains unclear whether insulin or glucose variations or both are primary determinants of circulating adrenal androgens in men because most of the reported relations with insulin have not been adjusted for anthropometric variables and plasma glucose. The question addressed by the present study was to evaluate the effect of hyperinsulinaemia and hyperglycaemia on serum adrenal steroid concentrations, independent of adiposity.
Over the past two decades, an abundant literature has focused on the adrenal androgens dehydroepiandrosterone sulphate (DHEAS) and dehydroepiandrosterone (DHEA) and their relation with immunity, ageing, obesity, diabetes and cardiovascular diseases in humans. Low levels of DHEAS predict cardiovascular mortality in men. It is known that type 2 diabetes is associated with a two- to fourfold higher risk of coronary heart disease (CHD) and lower levels of DHEAS than nondiabetic men. Whether these low circulating adrenal androgen levels are a primary phenomenon that links type 2 diabetes and CHD is questioned. At least three, main confounding factors may interfere (i.e. high adiposity, hyperinsulinism and hyperglycaemia). Adrenal androgen levels tend to be lower in overweight subjects and are associated with visceral fat accumulation. Although most but not all studies showed no association between fasting insulin concentrations and DHEAS or DHEA levels, experimentally induced hyperinsulinaemia was associated with decreased DHEA and DHEAS levels in healthy men. In addition, the lowering of fasting insulinaemia observed during diet-induced weight loss was associated with increased DHEAS levels in obese men. These findings suggest that insulin variations might influence DHEA and DHEAS levels in men. On the other hand, blood glucose levels itself might influence DHEAS and DHEA concentrations. For example, a negative correlation between the area under the plasma glucose curve during oral glucose tolerance test (OGTT) and serum DHEAS and DHEA levels was observed in Japanese men with impaired glucose tolerance and in normal glucose-tolerant Caucasians. DHEAS was also found to be inversely related with 2-h glucose in nondiabetic men. However, these correlations disappeared when the analysis accounted for adiposity. Thus, it remains unclear whether insulin or glucose variations or both are primary determinants of circulating adrenal androgens in men because most of the reported relations with insulin have not been adjusted for anthropometric variables and plasma glucose. The question addressed by the present study was to evaluate the effect of hyperinsulinaemia and hyperglycaemia on serum adrenal steroid concentrations, independent of adiposity.
