Cited time in webofscience Cited time in scopus

Hypothalamic AMPK-induced autophagy increases food intake by regulating NPY and POMC expression

Hypothalamic AMPK-induced autophagy increases food intake by regulating NPY and POMC expression
Oh, Tae SeokCho, HanchaeCho, Jae HyunYu, Seong-WoonKim, Eun-Kyoung
DGIST Authors
Yu, Seong-WoonKim, Eun-Kyoung
Issued Date
Article Type
UNC 51 Like Kinase 1ACTIVATED PROTEIN-KINASEAGRP NEURONSAnimal CellAnimal ExperimentAppetiteArticleAutophagyBODY-WEIGHTCell LineCOMPOUND CControlled StudyDeoxyglucoseDown RegulationENERGY-BALANCEEnzyme ActivationEnzyme InhibitionEnzyme PhosphorylationFATTY-ACIDFood IntakeGlucoprivationGLUCOSE-HOMEOSTASISGLUCOSE DEPRIVATIONHydroxymethylglutaryl Coenzyme A Reductase KinaseHyperphagiaHypothalamic AmpkHypothalamusHypothalamus NucleusIn Vitro StudyIn Vivo StudyKAPPA-BMaleMAMMALIAN TARGETMammalian Target of Rapamycin Complex 1MouseNeuropeptideNeuropeptide YNonhumanProopiomelanocortinProtein ExpressionProtein Serine Threonine KinaseRAT HYPOTHALAMUSUnclassified DrugWeight Reduction
Hypothalamic AMP-activated protein kinase (AMPK) plays important roles in the regulation of food intake by altering the expression of orexigenic or anorexigenic neuropeptides. However, little is known about the mechanisms of this regulation. Here, we report that hypothalamic AMPK modulates the expression of NPY (neuropeptide Y), an orexigenic neuropeptide, and POMC (pro-opiomelanocortin-α), an anorexigenic neuropeptide, by regulating autophagic activity in vitro and in vivo. In hypothalamic cell lines subjected to low glucose availability such as 2-deoxy-d-glucose (2DG)-induced glucoprivation or glucose deprivation, autophagy was induced via the activation of AMPK, which regulates ULK1 and MTOR complex 1 followed by increased Npy and decreased Pomc expression. Pharmacological or genetic inhibition of autophagy diminished the effect of AMPK on neuropeptide expression in hypothalamic cell lines. Moreover, AMPK knockdown in the arcuate nucleus of the hypothalamus decreased autophagic activity and changed Npy and Pomc expression, leading to a reduction in food intake and body weight. AMPK knockdown abolished the orexigenic effects of intraperitoneal 2DG injection by decreasing autophagy and changing Npy and Pomc expression in mice fed a high-fat diet. We suggest that the induction of autophagy is a possible mechanism of AMPK-mediated regulation of neuropeptide expression and control of feeding in response to low glucose availability. © 2016 Taylor & Francis.
Taylor and Francis Inc.
Related Researcher
  • 유성운 Yu, Seong-Woon 뇌과학과
  • Research Interests Molecular mechanisms of neuronal cell death and neurodegeneration
Files in This Item:

There are no files associated with this item.

Appears in Collections:
Department of Brain Sciences Lab of Neuro-Metabolism & Neurometabolomic Research Center 1. Journal Articles
Department of Brain Sciences Laboratory of Neuronal Cell Death 1. Journal Articles


  • twitter
  • facebook
  • mendeley

Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.