Journal
PLOS BIOLOGY
Volume 9, Issue 1, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pbio.1000575
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Funding
- National Institutes of Health (NIH) [R01 AG02792405, P01 AG03012801, HL20948, HL63762]
- Washington University DRTC [5P60DK020579]
- Alzheimer's Association
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL020948, R37HL063762, R01HL063762] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P60DK020579] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG035355, P01AG030128] Funding Source: NIH RePORTER
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Obesity is a growing epidemic characterized by excess fat storage in adipocytes. Although lipoprotein receptors play important roles in lipid uptake, their role in controlling food intake and obesity is not known. Here we show that the lipoprotein receptor LRP1 regulates leptin signaling and energy homeostasis. Conditional deletion of the Lrp1 gene in the brain resulted in an obese phenotype characterized by increased food intake, decreased energy consumption, and decreased leptin signaling. LRP1 directly binds to leptin and the leptin receptor complex and is required for leptin receptor phosphorylation and Stat3 activation. We further showed that deletion of the Lrp1 gene specifically in the hypothalamus by Cre lentivirus injection is sufficient to trigger accelerated weight gain. Together, our results demonstrate that the lipoprotein receptor LRP1, which is critical in lipid metabolism, also regulates food intake and energy homeostasis in the adult central nervous system.
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