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l-Carnitine Is a Modulator of the Glucocorticoid Receptor Alpha
aClinical Neuroendocrinology Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA bPediatric and Reproductive Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA cDepartment of Pharmacology, Faculty of Medicine, University of Patras, Rion-Patras, Greece
Address for correspondence: Salvatore Alesci, M.D., Ph.D., CNE/NIMH/NIH, 10 Center Drive, Bldg. 10, Rm. 2D46, MSC 1284, Bethesda, MD 20892-1284. Voice: 301-496-6886; fax: 301-402-1561. alescisa{at}mail.nih.gov Ann. N.Y. Acad. Sci. 1024: 147-152 (2004).
l-Carnitine (LC) is a nutrient with an essential role in cellular energy production. At high doses, LC can mimic some of the biological activities of glucocorticoids, particularly immunomodulation. To explore the molecular bases of this property, we tested the influence of LC on glucocorticoid receptor-a (GR
 ) functions. LC reduced the binding capacity of GR, induced its nuclear translocation, and stimulated its transcriptional activity. Moreover, LC suppressed TNF and IL-12 release from human monocytes in glucocorticoid-like fashion. We conclude that pharmacologic doses of LC can activate GR and, via this mechanism, regulate glucocorticoid-responsive genes, potentially sharing some of the biological and therapeutic properties of glucocorticoids.
Key Words: glucocorticoid receptor alpha • immunity • cytokines This article has been cited by other articles:
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