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Cell Metab. 2013 Jul 2;18(1):62-74. doi: 10.1016/j.cmet.2013.05.020.

Human but not mouse adipogenesis is critically dependent on LMO3.

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1
Department of Laboratory Medicine, Medical University of Vienna, 1090 Vienna, Austria.

Abstract

Increased visceral fat is associated with a high risk of diabetes and metabolic syndrome and is in part caused by excessive glucocorticoids (GCs). However, the molecular mechanisms remain undefined. We now identify the GC-dependent gene LIM domain only 3 (LMO3) as being selectively upregulated in a depot-specific manner in human obese visceral adipose tissue, localizing primarily in the adipocyte fraction. Visceral LMO3 levels were tightly correlated with expression of 11β-hydroxysteroid dehydrogenase type-1 (HSD11B1), the enzyme responsible for local activation of GCs. In early human adipose stromal cell differentiation, GCs induced LMO3 via the GC receptor and a positive feedback mechanism involving 11βHSD1. No such induction was observed in murine adipogenesis. LMO3 overexpression promoted, while silencing of LMO3 suppressed, adipogenesis via regulation of the proadipogenic PPARγ axis. These results establish LMO3 as a regulator of human adipogenesis and could contribute a mechanism resulting in visceral-fat accumulation in obesity due to excess glucocorticoids.

PMID:
23823477
PMCID:
PMC3701325
DOI:
10.1016/j.cmet.2013.05.020
[Indexed for MEDLINE]
Free PMC Article

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