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This version published online on March 17, 2005
Endocrinology, doi:10.1210/en.2005-0096
A more recent version of this article appeared on June 1, 2005
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*Substance via MeSH
Medline Plus Health Information
*Hormones

Submitted on January 24, 2005
Accepted on March 1, 2005

Regulation of Steroidogenesis by Electron Transfer

Walter L. Miller M.D.*

University of California San Francisco

Discussions of the regulation of steroidogenesis generally center on the CRH/ACTH/Glucocorticoid system and the Renin/Angiotensin/Mineralocorticoid system, which are classical examples of endocrine feedback loops regulated by circulating factors acting at a distance from their sites of synthesis. Recent work has expanded our understanding of steroidogenesis to include intracellular factors that directly influence steroidogenic enzymes. Perhaps the best-studied of these is the steroidogenic acute regulatory protein (StAR), which regulates the acute steroidogenic responses to ACTH and Angiotensin II (1, 2) by acting on the outer mitochondrial membrane (3). StAR increases the delivery of substrate (cholesterol) to the cholesterol side-chain cleavage enzyme, P450scc, but does not act on the enzyme itself. Another level of regulation is at the level of the catalytic efficiency of the steroidogenic enzymes themselves, which is regulated by electron transfer. Regulation of electron transfer to enzymes by complex electron transfer chains is a common cellular strategy for regulating many of biochemical processes, such as oxidative phosphorylation. Such biochemical regulation is also central to steroidogenic processes.




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