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Cell. 2015 Jan 15;160(1-2):88-104. doi: 10.1016/j.cell.2014.12.022.

Leptin and insulin act on POMC neurons to promote the browning of white fat.

Author information

1
Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia.
2
Department of Physiology, Monash University, Victoria 3800, Australia.
3
Pennington Biomedical Research Center, LSU Systems, Baton Rouge, LA 70808, USA.
4
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
5
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
6
Campbell Family Cancer Research Institute, Ontario Cancer Institute, Princess Margaret Hospital and Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada.
7
Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
8
Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia. Electronic address: tony.tiganis@monash.edu.

Abstract

The primary task of white adipose tissue (WAT) is the storage of lipids. However, "beige" adipocytes also exist in WAT. Beige adipocytes burn fat and dissipate the energy as heat, but their abundance is diminished in obesity. Stimulating beige adipocyte development, or WAT browning, increases energy expenditure and holds potential for combating metabolic disease and obesity. Here, we report that insulin and leptin act together on hypothalamic neurons to promote WAT browning and weight loss. Deletion of the phosphatases PTP1B and TCPTP enhanced insulin and leptin signaling in proopiomelanocortin neurons and prevented diet-induced obesity by increasing WAT browning and energy expenditure. The coinfusion of insulin plus leptin into the CNS or the activation of proopiomelanocortin neurons also increased WAT browning and decreased adiposity. Our findings identify a homeostatic mechanism for coordinating the status of energy stores, as relayed by insulin and leptin, with the central control of WAT browning.

PMID:
25594176
PMCID:
PMC4453004
DOI:
10.1016/j.cell.2014.12.022
[Indexed for MEDLINE]
Free PMC Article

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