Journal
SCIENCE
Volume 351, Issue 6279, Pages 1293-1296Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aad5494
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Funding
- NIH [R01NS036715, R01DK6167, N01-HV-00240, P01HL107153]
- National Institute on Drug Abuse Intramural Research Program
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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 alpha CaMKII-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 alpha CaMKII neurons of the PVN as an important molecular mechanism that regulates feeding behavior.
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