Will Brink
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DHEA: Does It Have Non-Hormonal Benefit?
Monica Mollica explores that topic via Brinkzone and it's a very interesting read:
DHEA (dehydroepiandrosterone) is most known for being a pro-hormone which in the body gets converted to testosterone and estrogen. It is a long held view that DHEA exerts all its effects via conversion to testosterone and estrogen. However, recent studies show that DHEA also has several interesting non-hormonal actions…
DHEA 101
DHEA is produced mainly by the adrenal cortex, and is rapidly sulfated by sulfotransferases into DHEA-S. DHEA and its sulfated form DHEA-S is the most abundant steroid (pro)hormone circulating in the blood stream.[1] The sulfated from of DHEA has a longer half-life in the blood and its levels remain stable throughout the day, are not altered significantly by the menstrual cycle. When getting a blood test for DHEA, the fraction that is routinely measured is therefore DHEA-S. In response to metabolic demand, DHEA-S is rapidly hydrolyzed back to DHEA by sulfatases.
DHEA levels decrease approximately 80% between ages 25 and 75 year.[2, 3] This large decline in DHEA spurred research interest in the possibility that aging related DHEA deficiency may play a role in the deterioration of physiological and metabolic functions with aging, and in the development of chronic diseases.
How does DHEA really work?
No specific cellular nuclear receptor has been identified for DHEA.[4] Therefore, the actions of DHEA have traditionally been thought to be mediated via conversion to testosterone and estradiol, which in turn activate androgen and estrogen receptors and thereby elicits their effects.[5-7] However, emerging research is showing that the action of DHEA also involves multiple other receptors, and that DHEA and /or its oxygenated metabolites, such as epiandrosterone (EpiA) metabolites.[8, 9]
Increased NO production
One DHEA activated receptor, a cell surface (membrane-bound) receptor, that binds DHEA with high affinity has been identified in the endothelium (blood vessel wall), heart, liver, and kidney.[10-13] This receptor is coupled to eNOS (endothelial nitric oxide synthase) [10-12], the enzyme that activates the synthesis of NO (nitric oxide).[14] Endothelial cells exposed to varying concentrations of DHEA produced dose-dependent increased activation of eNOS and elevated nitrate levels (a bi-product of NO).[10, 12] This activation of eNOS by DHEA was not inhibited by the antagonists of the estrogen, androgen, or progesterone receptors, suggesting that eNOS activation by DHEA was through a very specific receptor for DHEA.[12] Support for this comes from another study demonstrating that DHEA supplementation 50 g/day for 2 months in healthy men aged 58+ years increased cGMP (platelet cyclic guanosine-monophosphate) concentrations, which is a marker of NO production.[15]
DHEA also activates an important vascular endothelial cell signaling pathway (ERK1/2) which plays an important role in vascular function.[16] This, combined with the DHEA induced elevation in NO production could explain the beneficial cardiovascular effects which have been seen in several DHEA supplementation studies in humans; such as improvement in vascular endothelial function, arterial stiffness and insulin sensitivity. [17-20]
Cont:
DHEA - does it have any beneficial non-hormonal effects? | BrinkZone.com
Monica Mollica explores that topic via Brinkzone and it's a very interesting read:
DHEA (dehydroepiandrosterone) is most known for being a pro-hormone which in the body gets converted to testosterone and estrogen. It is a long held view that DHEA exerts all its effects via conversion to testosterone and estrogen. However, recent studies show that DHEA also has several interesting non-hormonal actions…
DHEA 101
DHEA is produced mainly by the adrenal cortex, and is rapidly sulfated by sulfotransferases into DHEA-S. DHEA and its sulfated form DHEA-S is the most abundant steroid (pro)hormone circulating in the blood stream.[1] The sulfated from of DHEA has a longer half-life in the blood and its levels remain stable throughout the day, are not altered significantly by the menstrual cycle. When getting a blood test for DHEA, the fraction that is routinely measured is therefore DHEA-S. In response to metabolic demand, DHEA-S is rapidly hydrolyzed back to DHEA by sulfatases.
DHEA levels decrease approximately 80% between ages 25 and 75 year.[2, 3] This large decline in DHEA spurred research interest in the possibility that aging related DHEA deficiency may play a role in the deterioration of physiological and metabolic functions with aging, and in the development of chronic diseases.
How does DHEA really work?
No specific cellular nuclear receptor has been identified for DHEA.[4] Therefore, the actions of DHEA have traditionally been thought to be mediated via conversion to testosterone and estradiol, which in turn activate androgen and estrogen receptors and thereby elicits their effects.[5-7] However, emerging research is showing that the action of DHEA also involves multiple other receptors, and that DHEA and /or its oxygenated metabolites, such as epiandrosterone (EpiA) metabolites.[8, 9]
Increased NO production
One DHEA activated receptor, a cell surface (membrane-bound) receptor, that binds DHEA with high affinity has been identified in the endothelium (blood vessel wall), heart, liver, and kidney.[10-13] This receptor is coupled to eNOS (endothelial nitric oxide synthase) [10-12], the enzyme that activates the synthesis of NO (nitric oxide).[14] Endothelial cells exposed to varying concentrations of DHEA produced dose-dependent increased activation of eNOS and elevated nitrate levels (a bi-product of NO).[10, 12] This activation of eNOS by DHEA was not inhibited by the antagonists of the estrogen, androgen, or progesterone receptors, suggesting that eNOS activation by DHEA was through a very specific receptor for DHEA.[12] Support for this comes from another study demonstrating that DHEA supplementation 50 g/day for 2 months in healthy men aged 58+ years increased cGMP (platelet cyclic guanosine-monophosphate) concentrations, which is a marker of NO production.[15]
DHEA also activates an important vascular endothelial cell signaling pathway (ERK1/2) which plays an important role in vascular function.[16] This, combined with the DHEA induced elevation in NO production could explain the beneficial cardiovascular effects which have been seen in several DHEA supplementation studies in humans; such as improvement in vascular endothelial function, arterial stiffness and insulin sensitivity. [17-20]
Cont:
DHEA - does it have any beneficial non-hormonal effects? | BrinkZone.com
