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

Yangsoo Jang, Jong Ho Lee, Yu Wang, Gary Sweeney

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

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. 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. 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.

Original languageEnglish
Pages (from-to)194-199
Number of pages6
JournalClinical and Experimental Pharmacology and Physiology
Volume39
Issue number2
DOIs
Publication statusPublished - 2012 Feb 1

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Insulin Resistance
Adipokines
Pandemics
C-Reactive Protein
Fasting
Body Mass Index
Homeostasis
Obesity
Inflammation
Glucose
Lipocalin-2
Serum
Therapeutics

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pharmacology
  • Physiology (medical)

Cite this

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Emerging clinical and experimental evidence for the role of lipocalin-2 in metabolic syndrome. / Jang, Yangsoo; Lee, Jong Ho; Wang, Yu; Sweeney, Gary.

In: Clinical and Experimental Pharmacology and Physiology, Vol. 39, No. 2, 01.02.2012, p. 194-199.

Research output: Contribution to journalArticle

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