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Regulation of Human Adipocyte Gene Expression by Thyroid Hormone

INSERM Unit 317 (N.V., L.M., S.A., D.Lar., D.Lan.), Institut Louis Bugnard, Université Paul Sabatier, Hôpital Rangueil, 31403 Toulouse Cedex 4, France; and INSERM Unit 449 (H.V.), Faculté de Médecine Laennec, 69372 Lyon Cedex 08, France

Address all correspondence and requests for reprints to: Dr. Nathalie Viguerie, INSERM U317, Institut Louis Bugnard, Btiment L3, Centre Hospitalier Universitaire Rangueil, 31403 Toulouse Cedex 4, France. E-mail: viguenat{at}rangueil inserm.fr.

Abstract

Thyroid hormones are key regulators of metabolism. In adipose tissue, changes in thyroid status result in alterations of lipolytic capacity. The effects of these hormones are mediated by thyroid hormone receptors that modulate gene transcription. Very few target genes have been identified in adipose tissue. To investigate the effect of T₃ on gene expression in human adipocytes, primary cultures of human sc adipose tissue explants were treated with T₃. ³²P-labeled cDNA probes prepared from isolated adipocyte total RNA were hybridized to cDNA arrays representing 1,176 genes. Among the statistically significant variations in mRNA levels with more than 1.3-fold difference, 13 and 6 genes were positively and negatively regulated, respectively (n = 3). The genes encoded proteins that were involved in signal transduction, lipid metabolism, apoptosis, and inflammatory response. Using RT-competitive PCR, we showed a down-regulation of phosphodiesterase 3B, _2A-adrenergic receptor, and G protein _i2 subunit mRNAs, and an up-regulation of ß₂-adrenergic receptor mRNA. These regulations may explain the T₃-mediated increase in catecholamine-induced lipolysis. The down-regulation of sterol regulatory element binding protein-1c, a transcription factor controlling lipogenic gene expression, may constitute a link between thyrotoxicosis and insulin resistance. Thus, these data suggest that T₃ modulates expression of genes with a wide range of function in human adipose tissue.

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