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

Research output: Contribution to journalArticlepeer-review

45 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)147-156
Number of pages10
JournalEndocrinology
Volume156
Issue number1
DOIs
Publication statusPublished - 2015 Jan 1

Bibliographical note

Publisher Copyright:
© 2015 by the Endocrine Society.

All Science Journal Classification (ASJC) codes

  • Endocrinology

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