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The Role of Lipocalin 2 in the Regulation of Inflammation in Adipocytes and Macrophages

Department of Food Science and Nutrition (J.Z., Y.Z., X.C.), University of Minnesota, St. Paul, Minnesota 55108-1038; and Department of Biochemistry, Molecular Biology and Biophysics (D.A.B.), University of Minnesota, Minneapolis, Minnesota 55455; Division of Endocrinology, Diabetes and Bone Disease (Y.W., D.L.), Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029

Address all correspondence and requests for reprints to: Dr. Xiaoli Chen, University of Minnesota, Food Science and Nutrition, Room 139, 1334 Eckles Avenue, St. Paul, Minnesota 55108-1038. E-mail: xlchen{at}umn.edu.

Adipose tissue-derived cytokines (adipokines) are associated with the development of inflammation and insulin resistance. However, which adipokine(s) mediate this linkage and the mechanisms involved during obesity is poorly understood. Through proteomics and microarray screening, we recently identified lipocalin 2 (LCN 2) as an adipokine that potentially connects obesity and its related adipose inflammation. Herein we show that the levels of LCN2 mRNA are dramatically increased in adipose tissue and liver of ob/ob mice and primary adipose cells isolated from Zucker obese rats, and thiazolidinedione administration reduces LCN2 expression. Interestingly, addition of LCN2 induces mRNA levels of peroxisome proliferator-activated receptor- (PPAR) and adiponectin. Reducing LCN2 gene expression causes decreased expression of PPAR and adiponectin, slightly reducing insulin-stimulated Akt2 phosphorylation at Serine 473 in 3T3-L1 adipocytes. LCN2 administration to 3T3-L1 cells attenuated TNF-effect on glucose uptake, expression of PPAR, insulin receptor substrate-1, and glucose transporter 4, and secretion of adiponectin and leptin. When added to macrophages, LCN2 suppressed lipopolysaccharide-induced cytokine production. Our data suggest that LCN2, as a novel autocrine and paracrine adipokine, acts as an antagonist to the effect of inflammatory molecules on inflammation and secretion of adipokines.

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