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Emerging clinical and experimental evidence for the role of lipocalin-2 in metabolic syndrome

Authors


  • This paper has been peer reviewed

Dr Gary Sweeney, Department of Biology, York University, Toronto, ON M3J 1P3, Canada. Email: gsweeney@yorku.ca.

Summary

1. The inflammatory state, which is associated with the current pandemic of obesity, has been established as an important contributing pathogenic factor to the increased prevalence of the so-called metabolic syndrome. Many studies have focused on the contribution of various adipokines to this phenomenon, and in the present study, we provide an update on the emerging evidence that the pro-inflammatory factor, lipocalin-2, might influence various aspects of metabolic syndrome.

2. Previous reports indicate a positive correlation of serum lipocalin-2 with fasting glucose, the homeostasis model assessment of insulin resistance index, and the inflammatory marker high-sensitivity C-reactive protein, even after adjustment for body mass index, suggesting that it is an independent risk factor for insulin resistance, diabetes, and inflammation. Direct analysis of lipocalin-2 action now also shows effects on peripheral metabolism and on cardiovascular function.

3. A better understanding of how lipocalin-2 is regulated locally and systemically is crucial for adding to our understanding of the pathogenesis of metabolic syndrome, and to uncover potential new avenues for therapeutic approaches.

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