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Corticotropin-Releasing Hormone System in Human Adipose Tissue

German Diabetes Center (J.S., P.S., W.A.S., M.E.-B.), Department of Endocrinology, Medical Center (S.R.B., H.S.W.), and Department of Surgery (K.M.S.), Heinrich Heine University of Duesseldorf, Duesseldorf 65 40225, Germany

Address all correspondence and requests for reprints to: Monika Ehrhart-Bornstein, Ph.D., German Diabetes Center, Auf’m Hennekamp 65, 40225 Düsseldorf, Germany. E-mail: ehrhart-bornstein{at}ddfi uni-duesseldorf.de.

Mounting evidence exists for a role of the CRH system in energy balance, including a direct influence on human adipocytes, the regulation of adipose 11ß-hydroxysteroid dehydrogenase type 1 activity, and cortisol formation. We characterized the expression of CRH receptors 1 and 2 and CRH-like peptides stresscopin and urocortin in human adipose tissue in comparison with other peripheral tissues, adrenal, and heart. The effect of CRH on CRH receptor and CRH-like peptide expression was analyzed in isolated human adipocytes using quantitative TaqMan PCR. CRH receptors were detectable in fat tissue at mRNA and protein levels. CRH-R2 expression in fat was comparable with its expression in the heart, the organ with the highest CRH-R2 expression known. CRH-R1:CRH-R2 ratio varied according to fat-depot type; whereas CRH-R1 expression was higher in sc fat than in visceral fat, the opposite was true for CRH-R2. Adipose tissue also expressed urocortin and stresscopin, the predominant ligands of peripheral CRH-R2. CRH down-regulated CRH-R1 and CRH-R2 mRNA expression in isolated adipocytes. These data, together with the recently published observation that CRH regulates adipocyte metabolism by down-regulating 11ß-hydroxysteroid dehydrogenase, indicate that a CRH system exists within human adipose tissue. This system could be implicated in energy homeostasis and in mediating the anorexic effects of CRH at adipose level.

This work was supported by the Deutsche Forschungsgemeinschaft (Grant Eh 161/2-4) (to M.E.-B.).

Abbreviations: CRH-R, CRH receptor; 11ß-HSD1, 11ß-hydroxysteroid dehydrogenase type 1.

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