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

 Jung-Hwan Baek  ;  Seok-Jun Kim  ;  Hyeok Gu Kang  ;  Hyun-Woo Lee  ;  Jung-Hoon Kim  ;  Kyung-A Hwang  ;  Jaewhan Song  ;  Kyung-Hee Chun 
 ENDOCRINOLOGY, Vol.156(1) : 147-156, 2015 
Journal Title
Issue Date
3T3-L1 Cells ; Adipocytes/cytology ; Adipocytes/metabolism ; Adipose Tissue, White/physiology* ; Adiposity ; Animals ; Cell Differentiation ; Dietary Fats/administration & dosage ; Dietary Fats/adverse effects* ; Dose-Response Relationship, Drug ; Female ; Galectin 3/genetics ; Galectin 3/metabolism* ; Gene Expression Regulation/physiology* ; HEK293 Cells ; Humans ; Male ; Mice ; Mice, Knockout ; Obesity/chemically induced* ; Obesity/metabolism ; PPAR gamma/genetics ; PPAR gamma/metabolism*
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.
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1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Seok Jun(김석준)
Baek, Jung Hwan(백정환) ORCID logo https://orcid.org/0000-0002-2250-1557
Chun, Kyung Hee(전경희) ORCID logo https://orcid.org/0000-0002-9867-7321
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