Ema
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DHEA has important benefits on oxidative energy metabolism as well as modulating cortisol.
It also increases levels of glutamate dehydrogenase. Glutamate is often elevated and neurotoxic due to activated microglial cells.
DHEA is also an antioxidant and may stimulate neurogenesis.
While too much is also not a good thing, leaving levels low for long periods of time seems counterproductive at best as well. I supplement DHEA at 25 mg a day; men can often use up to 50 mg/day successfully.
Optimal DHEA levels may be considered to be in the 4-500 ug/dl range for men and 350-430 for women.
It also increases levels of glutamate dehydrogenase. Glutamate is often elevated and neurotoxic due to activated microglial cells.
DHEA is also an antioxidant and may stimulate neurogenesis.
While too much is also not a good thing, leaving levels low for long periods of time seems counterproductive at best as well. I supplement DHEA at 25 mg a day; men can often use up to 50 mg/day successfully.
Optimal DHEA levels may be considered to be in the 4-500 ug/dl range for men and 350-430 for women.
Clin Biochem. 2007 Jan;40(1-2):57-65. Epub 2006 Sep 14.
Effect of dehydroepiandrosterone (DHEA) treatment on oxidative energy metabolism in rat liver and brain mitochondria. A dose-response study.
Patel MA1, Katyare SS.
Author information
Abstract
OBJECTIVES:
Effects of treatment with dehydroepiandrosterone (DHEA) on oxidative energy metabolism in rat liver and brain mitochondria were examined.
DESIGN AND METHODS:
Young adult rats were administered DHEA (0.1, 0.2, 1.0 or 2.0 mg/kg body weight) by subcutaneous route for 7 consecutive days.
RESULTS:
DHEA treatment resulted in general, in stimulation of state 3 respiration rates without having any uncoupling effect on ADP/O ratios. The stimulation of state 3 respiration rate for a given substrate was dose dependent in a tissue-specific manner. Parallel increases in the contents of cytochromes aa(3) and b were also noted. DHEA treatment stimulated the glutamate dehydrogenase (GDH) and succinate DCIP reductase (SDR) activities. Under the treatment conditions, mitochondrial ATPase activity was also stimulated.
CONCLUSIONS:
Treatment with DHEA significantly stimulated oxidative energy metabolism in liver and brain mitochondria.
PMID:
17052700
[PubMed - indexed for MEDLINE]
Neurochem Int. 2011 Sep;59(4):525-33. doi: 10.1016/j.neuint.2011.07.003. Epub 2011 Jul 13.
Glutamate dehydrogenase in brain mitochondria: do lipid modifications and transient metabolon formation influence enzyme activity?
McKenna MC1.
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Abstract
Metabolism of glutamate, the primary excitatory neurotransmitter in brain, is complex and of paramount importance to overall brain function. Thus, understanding the regulation of enzymes involved in formation and disposal of glutamate and related metabolites is crucial to understanding glutamate metabolism. Glutamate dehydrogenase (GDH) is a pivotal enzyme that links amino acid metabolism and TCA cycle activity in brain and other tissues. The allosteric regulation of GDH has been extensively studied and characterized. Less is known about the influence of lipid modifications on GDH activity, and the participation of GDH in transient heteroenzyme complexes (metabolons) that can greatly influence metabolism by altering kinetic parameters and lead to channeling of metabolites. This review summarizes evidence for palmitoylation and acylation of GDH, information on protein binding, and information regarding the participation of GDH in transient heteroenzyme complexes. Recent studies suggest that a number of other proteins can bind to GDH altering activity and overall metabolism. It is likely that these modifications and interactions contribute additional levels of regulation of GDH activity and glutamate metabolism.