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EMBO Rep. 2012 Mar 1;13(3):258-65. doi: 10.1038/embor.2011.260.

Loss of autophagy in hypothalamic POMC neurons impairs lipolysis.

Author information

1
Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

Abstract

Autophagy degrades cytoplasmic contents to achieve cellular homeostasis. We show that selective loss of autophagy in hypothalamic proopiomelanocortin (POMC) neurons decreases α-melanocyte-stimulating hormone (MSH) levels, promoting adiposity, impairing lipolysis and altering glucose homeostasis. Ageing reduces hypothalamic autophagy and α-MSH levels, and aged-mice phenocopy, the adiposity and lipolytic defect observed in POMC neuron autophagy-null mice. Intraperitoneal isoproterenol restores lipolysis in both models, demonstrating normal adipocyte catecholamine responsiveness. We propose that an unconventional, autophagosome-mediated form of secretion in POMC neurons controls energy balance by regulating α-MSH production. Modulating hypothalamic autophagy might have implications for preventing obesity and metabolic syndrome of ageing.

PMID:
22249165
PMCID:
PMC3323137
DOI:
10.1038/embor.2011.260
[Indexed for MEDLINE]
Free PMC Article

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