| First Author | Shechter R | Year | 2013 |
| Journal | Sci Rep | Volume | 3 |
| Pages | 1254 | PubMed ID | 23409245 |
| Mgi Jnum | J:207263 | Mgi Id | MGI:5554995 |
| Doi | 10.1038/srep01254 | Citation | Shechter R, et al. (2013) Hypothalamic neuronal toll-like receptor 2 protects against age-induced obesity. Sci Rep 3:1254 |
| abstractText | Toll-like receptors (TLRs) are traditionally associated with immune-mediated host defense. Here, we ascribe a novel extra-immune, hypothalamic-associated function to TLR2, a TLR-family member known to recognize lipid components, in the protection against obesity. We found that TLR2-deficient mice exhibited mature-onset obesity and susceptibility to high-fat diet (HFD)-induced weight gain, via modulation of food intake. Age-related obesity was still evident in chimeric mice, carrying comparable TLR2(+) immune cells, suggesting a non-hematopoietic-related involvement of this receptor. TLR2 was up-regulated with age or HFD in pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus, a brain area participating in central-metabolic regulation, possibly modulating the hypothalamic-anorexigenic peptide, alpha-melanocyte-stimulating hormone (alpha-MSH). Direct activation of TLR2 in a hypothalamic-neuronal cell-line via its known ligands, further supports its capacity to mediate non-immune related metabolic regulation. Thus, our findings identify TLR2 expressed by hypothalamic neurons as a potential novel regulator of age-related weight gain and energy expenditure. |
