| First Author | Guo H | Year | 2010 |
| Journal | Diabetes | Volume | 59 |
| Issue | 6 | Pages | 1376-85 |
| PubMed ID | 20332347 | Mgi Jnum | J:169355 |
| Mgi Id | MGI:4940471 | Doi | 10.2337/db09-1735 |
| Citation | Guo H, et al. (2010) Lipocalin-2 deficiency impairs thermogenesis and potentiates diet-induced insulin resistance in mice. Diabetes 59(6):1376-85 |
| abstractText | OBJECTIVE: Lipocalin (LCN) 2 belongs to the lipocalin subfamily of low-molecular mass-secreted proteins that bind small hydrophobic molecules. LCN2 has been recently characterized as an adipose-derived cytokine, and its expression is upregulated in adipose tissue in genetically obese rodents. The objective of this study was to investigate the role of LCN2 in diet-induced insulin resistance and metabolic homeostasis in vivo. RESEARCH DESIGN AND METHODS: Systemic insulin sensitivity, adaptive thermogenesis, and serum metabolic and lipid profile were assessed in LCN2-deficient mice fed a high-fat diet (HFD) or regular chow diet. RESULTS: The molecular disruption of LCN2 in mice resulted in significantly potentiated diet-induced obesity, dyslipidemia, fatty liver disease, and insulin resistance. LCN2(-/-) mice exhibit impaired adaptive thermogenesis and cold intolerance. Gene expression patterns in white and brown adipose tissue, liver, and muscle indicate that LCN2(-/-) mice have increased hepatic gluconeogenesis, decreased mitochondrial oxidative capacity, impaired lipid metabolism, and increased inflammatory state under the HFD condition. CONCLUSIONS: LCN2 has a novel role in adaptive thermoregulation and diet-induced insulin resistance. |
