2006
DOI: 10.1016/j.steroids.2006.04.001
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Dehydroepiandrosterone inhibits intracellular calcium release in β-cells by a plasma membrane-dependent mechanism

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Cited by 18 publications
(7 citation statements)
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“…Steroids coupled to BSA or other large proteins have been used extensively to characterize plasma membrane-initiated signaling (47)(48)(49)(50)(51). Whereas dissociation of steroid-BSA complexes with increased free steroid has been reported (52), there was no detectable free DHEA in the DHEA-BSA used in the present study (53). Collectively, our findings are consistent with a plasma membrane, Gi protein-coupled DHEA receptor.…”
Section: Discussionsupporting
confidence: 89%
“…Steroids coupled to BSA or other large proteins have been used extensively to characterize plasma membrane-initiated signaling (47)(48)(49)(50)(51). Whereas dissociation of steroid-BSA complexes with increased free steroid has been reported (52), there was no detectable free DHEA in the DHEA-BSA used in the present study (53). Collectively, our findings are consistent with a plasma membrane, Gi protein-coupled DHEA receptor.…”
Section: Discussionsupporting
confidence: 89%
“…On the other hand, dehydroepiandrosterone decreased agonist-induced Ca2+ release by a rapid, non-genomic mechanism in INS-1 cells, and inhibited insulin secretion induced by carbachol (an agonist of insulin secretion). These data provides evidence in concert with the existence of a specific plasma membrane dehydroepiandrosterone receptor, mediating this signal transduction pathway by G proteins [92].…”
Section: Effects Of Androgens On the Endocrine Pancreasmentioning
confidence: 55%
“…On the basis of mRNA expression, Valle et al (2006) demonstrate that human adipose tissue is capable of taking up DHEAS using specific OAT and OATP (organic anion-transporting polypeptide) transporters, as well as exhibiting the necessary enzymes, including steroid sulfatase (STS), to metabolize DHEAS into DHEA, thought to be the active form, within the cells. DHEA has also been shown to inhibit the glucose-stimulated releases of insulin from human beta cells at physiological doses (Liu et al 2006), potentially decreasing the uptake of glucose by muscle and increasing its uptake by adipose cells.…”
Section: Adrenarche and Somatic Glucose Metabolismmentioning
confidence: 99%