Introduction: Obesity is characterized by an expanded and chronically inflamed adipose tissue (AT). The galectin (Gal) family of proteins exerts a variety of activities, including regulation of inflammation and adipogenesis.
Methods: We used RT-PCR, ELISA and flow cytometry to evaluate regulation of expression and production of 4 members of the Gal family Gal1, Gal3, Gal9 and Gal12 in visceral (VAT) and subcutaneous (SAT) adipose tissue of male C57BL6 mice fed a low (LFD) or high fat diet (HFD) for 5, 9, 13, 17 and 24 weeks.
Results: Feeding a HFD induced a progressive elevation in body weight and circulating leptin levels that was accompanied by a significant increase in serum levels of Gal1 and Gal3. Expression of each of the 4 Gal did not significantly change over time in either VAT or SAT of LFD mice. In mice fed a HFD there was a progressive and significant increase in expression of the anti-inflammatory Gal1 and Gal9 selectively in SAT, whereas expression of the pro-inflammatory Gal3 significantly increased in both VAT and SAT of HFD-fed mice. Expression of Gal12, which modulates adipogenesis, significantly declined over time in VAT, but not SAT, of HFD mice, following a trend comparable to adiponectin. Evaluation of cellular expression indicated that both adipocytes and the stromovascular fraction (SVF) produced Gal1 and Gal3, while Gal9 was predominantly produced by the SVF and Gal12 almost exclusively by adipocytes. Flow cytometry analysis demonstrated increased production of Gal3 and Gal9, but not Gal1, in both CD11c− and CD11c+ macrophages obtained from VAT, but not SAT, of HFD versus LFD mice.Conclusions: Our data indicate that feeding a HFD leads to differential modulation of Gal1, Gal3, Gal9 and Gal12 in macrophages and adipocytes in VAT and SAT, suggesting that Gal proteins may actively participate in regulating inflammation and adipogenesis in obesity.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details are unavailable.
05 - 09 May 2012
European Society of Endocrinology