| First Author | Mosialou I | Year | 2020 |
| Journal | J Exp Med | Volume | 217 |
| Issue | 10 | PubMed ID | 32639539 |
| Mgi Jnum | J:298706 | Mgi Id | MGI:6477204 |
| Doi | 10.1084/jem.20191261 | Citation | Mosialou I, et al. (2020) Lipocalin-2 counteracts metabolic dysregulation in obesity and diabetes. J Exp Med 217(10) |
| abstractText | Regulation of food intake is a recently identified endocrine function of bone that is mediated by Lipocalin-2 (LCN2). Osteoblast-secreted LCN2 suppresses appetite and decreases fat mass while improving glucose metabolism. We now show that serum LCN2 levels correlate with insulin levels and beta-cell function, indices of healthy glucose metabolism, in obese mice and obese, prediabetic women. However, LCN2 serum levels also correlate with body mass index and insulin resistance in the same individuals and are increased in obese mice. To dissect this apparent discrepancy, we modulated LCN2 levels in mice. Silencing Lcn2 expression worsens metabolic dysfunction in genetic and diet-induced obese mice. Conversely, increasing circulating LCN2 levels improves metabolic parameters and promotes beta-cell function in mouse models of beta-cell failure acting as a growth factor necessary for beta-cell adaptation to higher metabolic load. These results indicate that LCN2 up-regulation is a protective mechanism to counteract obesity-induced glucose intolerance by decreasing food intake and promoting adaptive beta-cell proliferation. |
