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Open Access Review

Regulation of triglyceride metabolism by glucocorticoid receptor

Jen-Chywan Wang123*, Nora E Gray12, Taiyi Kuo13 and Charles A Harris45

Author Affiliations

1 Department of Nutritional Science & Toxicology, University of California at Berkeley, Berkeley, CA, 94720, USA

2 Graduate Program of Metabolic Biology, University of California at Berkeley

3 Graduate Program of Endocrinology, University of California at Berkeley

4 Gladstone Institute for Cardiovascular Disease, , San Francisco, CA, 94158, USA

5 Department of Medicine, University of California, San Francisco, CA, 94143, USA

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Cell & Bioscience 2012, 2:19  doi:10.1186/2045-3701-2-19

Published: 28 May 2012

Abstract

Glucocorticoids are steroid hormones that play critical and complex roles in the regulation of triglyceride (TG) homeostasis. Depending on physiological states, glucocorticoids can modulate both TG synthesis and hydrolysis. More intriguingly, glucocorticoids can concurrently affect these two processes in adipocytes. The metabolic effects of glucocorticoids are conferred by intracellular glucocorticoid receptors (GR). GR is a transcription factor that, upon binding to glucocorticoids, regulates the transcriptional rate of specific genes. These GR primary target genes further initiate the physiological and pathological responses of glucocorticoids. In this article, we overview glucocorticoid-regulated genes, especially those potential GR primary target genes, involved in glucocorticoid-regulated TG metabolism. We also discuss transcriptional regulators that could act with GR to participate in these processes. This knowledge is not only important for the fundamental understanding of steroid hormone actions, but also are essential for future therapeutic interventions against metabolic diseases associated with aberrant glucocorticoid signaling, such as insulin resistance, dyslipidemia, central obesity and hepatic steatosis.

Keywords:
Glucocorticoid; Glucocorticoid receptor; Triglyceride; Lipogenesis; Lipolysis; Glucocorticoid response Element; Transcription