Re: Acne-----HPA axis-----and CRH

[Guest guest]

Interesting. CRH induces sebum production. Cortisol ameliorates

acne. Testosterone and GH induce sebum production, yet negatively

inhibit CRH. Wonder which effect outweighs the other. It's so

confusing to think about, especially when I haven't eaten enough

omega-3 EFA in my diet...

> Physiology

> Corticotropin-releasing hormone: An autocrine hormone that promotes

lipogenesis in human sebocytes

> Christos C. Zouboulis*,, Holger Seltmann*, Naoki Hiroi,§, WenChieh

Chen¶, Maggie Young§, Marina Oeff*, Werner A. Scherbaum, Constantin

E. Orfanos*, M. McCann, and Stefan R. Bornstein,§

> * Department of Dermatology, University Medical Center

lin, The Free University of Berlin, 14195 Berlin, Germany;

Department of Endocrinology, University Medical Center, Heinrich

Heine University of Duesseldorf, 40225 Duesseldorf, Germany; §

Pediatric and Reproductive Endocrinology Branch, National Institute

of Child Health and Development, National Institutes of Health,

Bethesda, MD 20892-1583; ¶ Department of Dermatology, College of

Medicine, National Cheng Kung University, 704 Tainan, Taiwan; and

Pennington Biomedical Research Center, Baton Rouge, LA 70808-4124

> Contributed by M. McCann, March 27, 2002

>

> Sebaceous glands may be involved in a pathway conceptually similar

to that of the hypothalamic-pituitary-adrenal (HPA) axis. Such a

pathway has been described and may occur in human skin and lately in

the sebaceous glands because they express neuropeptide receptors.

Corticotropin-releasing hormone (CRH) is the most proximal element of

the HPA axis, and it acts as central coordinator for neuroendocrine

and behavioral responses to stress. To further examine the

probability of an HPA equivalent pathway, we investigated the

expression of CRH, CRH-binding protein (CRH-BP), and CRH receptors

(CRH-R) in SZ95 sebocytes in vitro and their regulation by CRH and

several other hormones. CRH, CRH-BP, CRH-R1, and CRH-R2 were

detectable in SZ95 sebocytes at the mRNA and protein levels: CRH-R1

was the predominant type (CRH-R1/CRH-R2 = 2). CRH was biologically

active on human sebocytes: it induced biphasic increase in synthesis

of sebaceous lipids with a maximum stimulation at 107 M and up-

regulated mRNA levels of 3- hydroxysteroid dehydrogenase/5-4

isomerase, although it did not affect cell viability, cell

proliferation, or IL-1-induced IL-8 release. CRH,

dehydroepiandrosterone, and 17-estradiol did not modulate CRH-R

expression, whereas testosterone at 107 M down-regulated CRH-R1 and

CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched

CRH-R1 mRNA expression to CRH-R2 at 24 h. Based on these findings,

CRH may be an autocrine hormone for human sebocytes that exerts

homeostatic lipogenic activity, whereas testosterone and growth

hormone induce CRH negative feedback. The findings implicate CRH in

the clinical development of acne, seborrhea, androgenetic alopecia,

skin aging, xerosis, and other skin disorders associated with

alterations in lipid formation of sebaceous origin.

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