Horm Metab Res 2010; 42(11): 787-791
DOI: 10.1055/s-0030-1262854
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Modulation of IGFBP2 mRNA Expression in White Adipose Tissue upon Aging and Obesity

Z. Li1 , F. Picard1
  • 1Centre de recherche de l’Institut universitaire de cardiologie et de pneumologie de Québec, Laval University, Québec, QC, Canada G1V 4G5
Further Information

Publication History

received 19.03.2010

accepted 12.07.2010

Publication Date:
20 August 2010 (online)

Abstract

The insulin/IGF-1 signaling pathway is a determinant of aging and age-related diseases. IGF-binding protein 2 (IGFBP2) is secreted by white adipocytes and contributes to the prevention of diet-induced obesity and age-related insulin resistance in mice. However, the expression levels of IGFBP2 in insulin resistance disorders have not been evaluated. The present study was aimed at determining IGFBP2 mRNA levels in adipose tissue in conditions of insulin resistance such as aging and obesity. In visceral white adipose tissue (WAT), but not in subcutaneous WAT, IGFBP2 mRNA levels were significantly lower in obese ob/ob, db/db and high fat-fed mice compared with those of their respective lean and chow-fed littermates. IGFBP2 mRNA levels were also decreased in visceral WAT of 12 and 24 months old mice compared with those of their 4 months old counterparts. Visceral WAT IGFBP2 expression was significantly associated with IGFBP2 circulating levels in mice, suggesting an important contribution from this tissue. The negative effect of aging on IGFBP2 mRNA levels in visceral WAT was confirmed in obese men. These findings demonstrate that the transcription of the IGFBP2 gene is modulated in a depot-specific fashion in obesity and aging in mice and men. Because IGFBP2 is an adipokine, an altered production from visceral WAT depots could impact on IGF-1 signaling and its downstream targets. This supports the need for further molecular and clinical studies to determine the factors regulating IGFBP2 expression and its relevance to metabolicdiseases.

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Correspondence

F. Picard

Institut universitaire de

cardiologie et de pneumologie

de Québec (IUCPQ)

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Canada

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Email: Frederic.Picard@criucpq.ulaval.ca