The nutrient sensor OGT in PVN neurons regulates feeding

Author:

Lagerlöf Olof12,Slocomb Julia E.3,Hong Ingie1,Aponte Yeka14,Blackshaw Seth1,Hart Gerald W.2,Huganir Richard L.1

Affiliation:

1. Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

2. Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

3. National Institute on Drug Abuse + National Institutes of Health/Johns Hopkins University Graduate Partnership Program, Baltimore, MD 21224, USA.

4. Intramural Research Program, Neuronal Circuits and Behavior Unit, National Institute on Drug Abuse, Baltimore, MD 21224, USA.

Abstract

When enough isn't enough Overeating and obesity are rapidly becoming worldwide problems. Normally, mice do not overeat—they balance their caloric intake with their caloric needs. Lagerlöf et al. deleted an enzyme called O-GlcNAc transferase (OGT) from a subset of neurons in the mouse hypothalamus (see the Perspective by Schwartz). After the loss of OGT, the animals began to overeat and rapidly gained weight. The animals ate more at meal times, rather than eating more often. Thus, OGT seems to regulate satiety and helps to couple caloric intake to caloric need. Science , this issue p. 1293 ; see also p. 1268

Funder

NIH

National Institute on Drug Abuse Intramural Research Program

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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