AI Article Synopsis
- Orexin A (OX) is a neuropeptide hormone that plays a key role in stimulating feeding, wakefulness, and energy expenditure through its receptors OXR1 and OXR2.
- Mice lacking OX are prone to obesity and exhibit problems with brown adipose tissue (BAT) development, starting from fetal growth, even though they eat less.
- The study indicates that the differentiation and energy regulation issues in OX-deficient models are primarily linked to the absence of OXR1, highlighting its critical role in temperature and obesity regulation.
Article Abstract
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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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661127 | PMC |
| http://dx.doi.org/10.4161/adip.18965 | DOI Listing |
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