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Lipocalin-2 deficiency impairs thermogenesis and potentiates diet-induced insulin resistance in mice.

Authors: Guo, Hong  Jin, Daozhong  Zhang, Yuanyuan  Wright, Wendy  Bazuine, Merlijn  Brockman, David A  Bernlohr, David A  Chen, Xiaoli 
Citation: Guo H, etal., Diabetes. 2010 Jun;59(6):1376-85. doi: 10.2337/db09-1735. Epub 2010 Mar 23.
Pubmed: (View Article at PubMed) PMID:20332347
DOI: Full-text: DOI:10.2337/db09-1735

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.


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RGD Object Information
RGD ID: 13673743
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.