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Orexin receptor-1 mediates brown fat developmental differentiation.

Authors: Sellayah, Dyan  Sikder, Devanjan 
Citation: Sellayah D and Sikder D, Adipocyte. 2012 Jan 1;1(1):58-63. doi: 10.4161/adip.18965.
Pubmed: (View Article at PubMed) PMID:23700511
DOI: Full-text: DOI:10.4161/adip.18965

Orexin A (OX) is a small excitatory neuropeptide hormone that stimulates feeding, wakefulness and energy expenditure via a pair of G-coupled protein receptors, namely orexin receptor-1 (OXR1) and orexin receptor-2 (OXR2). OX-deficient mice are sensitive to obesity despite being hypophagic. The obesogenic effect of OX-deletion is due to brown adipose tissue (BAT) dysfunction, a defect that originates during fetal growth. Brown preadipocytes in OX-null mice display undifferentiated histological appearance and fail to support both diet- and cold-induced thermogenesis. We show that the OXR1-null mice phenocopies the differentiation defect observed in the ligand-null mice indicating that OXR1 relays OX's differentiation and thermogenic function. Consistent with this, OX fails to induce differentiation in cultured OXR1-null preadipocytes. Thus, OX signaling via OXR1 constitutes an important thermoregulatory mechanism that defends against cold and obesity.

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RGD ID: 13673843
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE



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