Loss of autophagy in hypothalamic POMC neurons impairs lipolysis

Susmita Kaushik, Esperanza Arias, Hyok Joon Kwon, Nuria Martinez-Lopez, Diana Athonvarangkul, Srabani Sahu, Gary J. Schwartz, Jeffrey E. Pessin, Rajat Singh

Research output: Contribution to journalArticlepeer-review

133 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)258-265
Number of pages8
JournalEMBO Reports
Issue number3
StatePublished - Mar 2012


  • POMC
  • ageing
  • autophagy
  • hypothalamus
  • obesity

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics


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