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This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: 293/1/E364    most recent 00054.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Sjögren, K. Articles by Ho, K. K. Y. Search for Related Content PubMed PubMed Citation Articles by Sjögren, K. Articles by Ho, K. K. Y.

Growth hormone regulation of metabolic gene expression in muscle: a microarray study in hypopituitary men

¹Pituitary Research Unit, ²Peter Wills Bioinformatics Centre, and ³Cancer Research Program, Garvan Institute of Medical Research, Sydney; ⁴Department of Endocrinology, St Vincent's Hospital, Sydney, New South Wales, Australia; ⁵Division of Endocrinology, Department of Internal Medicine, Sahlgrenska Academy at Göteborg University, Gothenburg, Sweden

Submitted 22 January 2007 ; accepted in final form 18 April 2007

Muscle is a target of growth hormone (GH) action and a major contributor to whole body metabolism. Little is known about how GH regulates metabolic processes in muscle or the extent to which muscle contributes to changes in whole body substrate metabolism during GH treatment. To identify GH-responsive genes that regulate substrate metabolism in muscle, we studied six hypopituitary men who underwent whole body metabolic measurement and skeletal muscle biopsies before and after 2 wk of GH treatment (0.5 mg/day). Transcript profiles of four subjects were analyzed using Affymetrix GeneChips. Serum insulin-like growth factor I (IGF-I) and procollagens I and III were measured by RIA. GH increased serum IGF-I and procollagens I and III, enhanced whole body lipid oxidation, reduced carbohydrate oxidation, and stimulated protein synthesis. It induced gene expression of IGF-I and collagens in muscle. GH reduced expression of several enzymes regulating lipid oxidation and energy production. It reduced calpain 3, increased ribosomal protein L38 expression, and displayed mixed effects on genes encoding myofibrillar proteins. It increased expression of circadian gene CLOCK, and reduced that of PERIOD. In summary, GH exerted concordant effects on muscle expression and blood levels of IGF-I and collagens. It induced changes in genes regulating protein metabolism in parallel with a whole body anabolic effect. The discordance between muscle gene expression profiles and metabolic responses suggests that muscle is unlikely to contribute to GH-induced stimulation of whole body energy and lipid metabolism. GH may regulate circadian function in skeletal muscle by modulating circadian gene expression with possible metabolic consequences.

substrate metabolism; metabolic genes; transcript profiling