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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, TS[Oh, Tae Seok]Cho, H[Cho, Hanchae]Cho, JH[Cho, Jae Hyun]Yu, SW[Yu, Seong-Woon]Kim, EK[Kim, Eun-Kyoung]
DGIST Authors
Oh, TS[Oh, Tae Seok]; Cho, H[Cho, Hanchae]; Cho, JH[Cho, Jae Hyun]; Yu, SW[Yu, Seong-Woon]Kim, EK[Kim, Eun-Kyoung]
Issue Date
Autophagy, 12(11), 2009-2025
Article Type
Animal CellAnimal ExperimentAppetiteAutophagyCell LineControlled StudyDeoxyglucoseDown-RegulationEnzyme ActivationEnzyme InhibitionEnzyme PhosphorylationFood IntakeGlucoprivationGlucose DeprivationHydroxymethylglutaryl Coenzyme A Reductase KinaseHyperphagiaHypothalamic AMPKHypothalamusHypothalamus NucleusIn Vitro StudyIn Vivo StudyMaleMammalian Target of Rapamycin Complex 1MouseNeuropeptideNeuropeptide YNon-HumanProopiomelanocortinProtein ExpressionProtein Serine Threonine KinaseUNC 51 Like Kinase 1Unclassified 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
  • Author Yu, Seong-Woon Laboratory of Neuronal Cell Death
  • Research Interests Molecular mechanisms of neuronal cell death and neurodegeneration
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Department of Brain and Cognitive SciencesLaboratory of Neuronal Cell Death1. Journal Articles
Department of Brain and Cognitive SciencesLab of Neuro-Metabolism & Neurometabolomic Research Center1. Journal Articles

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