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.
Original language | English (US) |
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Pages (from-to) | 258-265 |
Number of pages | 8 |
Journal | EMBO Reports |
Volume | 13 |
Issue number | 3 |
DOIs | |
State | Published - Mar 2012 |
Keywords
- POMC
- ageing
- autophagy
- hypothalamus
- obesity
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Genetics