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The nutrient sensor OGT in PVN neurons regulates feeding
Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD, USA. (Olof Lagerlöf)
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2016 (Engelska)Ingår i: Science, ISSN 0036-8075, E-ISSN 1095-9203, Vol. 351, nr 6279, s. 1293-1296Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Maintaining energy homeostasis is crucial for the survival and health of organisms. The brain regulates feeding by responding to dietary factors and metabolic signals from peripheral organs. It is unclear how the brain interprets these signals. O-GlcNAc transferase (OGT) catalyzes the posttranslational modification of proteins by O-GlcNAc and is regulated by nutrient access. Here, we show that acute deletion of OGT from αCaMKII-positive neurons in adult mice caused obesity from overeating. The hyperphagia derived from the paraventricular nucleus (PVN) of the hypothalamus, where loss of OGT was associated with impaired satiety. These results identify O-GlcNAcylation in αCaMKII neurons of the PVN as an important molecular mechanism that regulates feeding behavior.

Ort, förlag, år, upplaga, sidor
AAAS , 2016. Vol. 351, nr 6279, s. 1293-1296
Nationell ämneskategori
Neurovetenskaper
Identifikatorer
URN: urn:nbn:se:umu:diva-182712DOI: 10.1126/science.aad5494ISI: 000372397700036PubMedID: 26989246Scopus ID: 2-s2.0-84961734214OAI: oai:DiVA.org:umu-182712DiVA, id: diva2:1548791
Tillgänglig från: 2021-05-03 Skapad: 2021-05-03 Senast uppdaterad: 2021-05-04Bibliografiskt granskad

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