Journal
SCIENCE
Volume 364, Issue 6447, Pages 1271-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aax1184
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Funding
- National Institutes of Health [NIDDK DK112564, NIMH MH093315, MH115165, NS007431, NIDA DA041184, DA038168, DA032750]
- Foundation of Hope
- Brain and Behavior Research Foundation (NARSAD)
- UNC Neuroscience Center Microscopy Core [P30 NS045892]
- Swedish Research Council (VR) [538-2013-8864]
- Swiss National Science Foundation
- National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust
- King's College London
- GSTT Charity [TR130505]
- Maudsley Charity [980]
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The current obesity epidemic is a major worldwide health concern. Despite the consensus that the brain regulates energy homeostasis, the neural adaptations governing obesity are unknown. Using a combination of high-throughput single-cell RNA sequencing and longitudinal in vivo two-photon calcium imaging, we surveyed functional alterations of the lateral hypothalamic area (LHA)-a highly conserved brain region that orchestrates feeding-in a mouse model of obesity. The transcriptional profile of LHA glutamatergic neurons was affected by obesity, exhibiting changes indicative of altered neuronal activity. Encoding properties of individual LHA glutamatergic neurons were then tracked throughout obesity, revealing greatly attenuated reward responses. These data demonstrate how diet disrupts the function of an endogenous feeding suppression system to promote overeating and obesity.
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