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Endocrinology. 2015 Jan;156(1):147-56. doi: 10.1210/en.2014-1374.

Galectin-3 activates PPARγ and supports white adipose tissue formation and high-fat diet-induced obesity.

Author information

1
Department of Biochemistry and Molecular Biology (J.-H.B., S.-J.K., H.G.K., H.-W.L., K.-H.C.), Yonsei University College of Medicine, Seodaemun-gu, Seoul 120-752, Republic of Korea; Department of Biochemistry (H.-W.L., J.-H.K., J.S.), College of Life Science and Biotechnology, and Brain Korea 21 PLUS Project for Medical Science (J.-H.B., S.-J.K., H.G.K., K.-H.C.), Yonsei University, Seoul 120-749, Republic of Korea; and Department of Agrofood Resources (K.-A.H.), National Academy of Agricultural Science, Rural Development Administration, Suwon 441-857, Republic of Korea.

Abstract

Galectin-3, a β-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)-γ, ccaat-enhancer-binding protein α, and ccaat-enhancer-binding protein β. Endogenous galectin-3 directly interacted with PPARγ, and galectin-3 ablation reduced the nuclear accumulation and transcriptional activation of PPARγ. 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 PPARγ and other lipogenic genes was drastically decreased in the eWAT and liver of lgals3(-/-) mice. We suggest that galectin-3 directly activates PPARγ and leads to adipocyte differentiation in vitro and in vivo. Furthermore, galectin-3 might be a potential therapeutic target in metabolic syndromes as a PPARγ regulator.

PMID:
25343273
DOI:
10.1210/en.2014-1374
[Indexed for MEDLINE]

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