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Lipocalin 2 is an important regulator of lipid metabolism and energy utilization
Author(s) -
Zhang Yuanyuan,
Guo Hong,
Chen Xiaoli
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.105.1
Subject(s) - endocrinology , medicine , lipolysis , lipocalin , brown adipose tissue , glycogen , thermogenin , lipid metabolism , biology , thermogenesis , energy homeostasis , adipose tissue , chemistry , obesity
We have recently identified lipocalin 2 (LCN2) as an adipose‐derived cytokine playing a critical role in thermoregulation. In this study, we further explored the efficiency of energy utilization in response to acute cold exposure in Lcn2−/− mice. We found that after exposed to 4°C for 5hs, Lcn2−/− mice developed significantly lower blood glucose levels compared with wild type (WT) mice. The liver and muscle glycogen contents were markedly reduced, while serum fatty acid and lactate levels were significantly higher in Lcn2−/− mice compared to WT mice after 5h cold exposure. The gene expression patterns in brown adipose tissue and muscle showed that cold‐induced expression of PGC1α and UCP1 was not different between WT and Lcn2−/− mice. Compared to WT, Lcn2−/− mice had significantly lower mRNA expression of mitochondrial function‐related genes Nrf1, EERα, COXiv, and ATP5β in BAT and muscle. Furthermore, Lcn2−/− WAT had higher levels of cold‐induced HSL phosphorylation than WT WAT indicating an increased lipolysis in Lcn2−/− mice. TZD treatment completely rescued cold intolerance and reversed serum parameters and mitochondrial gene expression. Our results suggest that LCN2 deficiency impairs mitochondrial function and lipid utilization leading to decreased energy production and cold intolerance. Thus, we conclude that LCN2 has a key role in lipid metabolism and energy utilization.