| First Author | Baek JH | Year | 2015 |
| Journal | Endocrinology | Volume | 156 |
| Issue | 1 | Pages | 147-56 |
| PubMed ID | 25343273 | Mgi Jnum | J:219662 |
| Mgi Id | MGI:5629468 | Doi | 10.1210/en.2014-1374 |
| Citation | Baek JH, et al. (2015) Galectin-3 activates PPARgamma and supports white adipose tissue formation and high-fat diet-induced obesity. Endocrinology 156(1):147-56 |
| abstractText | Galectin-3, a beta-galactoside-binding lectin, is elevated in obesity and type 2 diabetes mellitus, and metformin treatment reduces these galectin-3 levels. However, the role of galectin-3 in adipogenesis remains controversial. We found that 17-month-old galectin-3-deficient (lgals3(-/-)) mice had decreased body size and epididymal white adipose tissue (eWAT) without related inflammatory diseases when fed normal chow. Galectin-3 knockdown significantly reduced adipocyte differentiation in 3T3-L1 cells and also decreased the expression of peroxisome proliferator-activated receptor (PPAR)-gamma, ccaat-enhancer-binding protein alpha, and ccaat-enhancer-binding protein beta. Endogenous galectin-3 directly interacted with PPARgamma, and galectin-3 ablation reduced the nuclear accumulation and transcriptional activation of PPARgamma. After a 12-week high-fat diet (60% fat), lgals3(-/-) mice had lower body weight and eWAT mass than lgals3(+/+) mice. Moreover, the expression of PPARgamma and other lipogenic genes was drastically decreased in the eWAT and liver of lgals3(-/-) mice. We suggest that galectin-3 directly activates PPARgamma and leads to adipocyte differentiation in vitro and in vivo. Furthermore, galectin-3 might be a potential therapeutic target in metabolic syndromes as a PPARgamma regulator. |
