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 journalArticle

31 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

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Galectin 3
White Adipose Tissue
Peroxisome Proliferator-Activated Receptors
High Fat Diet
Obesity
Adipocytes
Carrier Proteins
3T3-L1 Cells
Galactosides
Adipogenesis
Metformin
Body Size
Lectins
Type 2 Diabetes Mellitus
Transcriptional Activation
Fats
Body Weight

All Science Journal Classification (ASJC) codes

  • Endocrinology

Cite this

Baek, J. H., Kim, S. J., Kang, H. G., Lee, H. W., Kim, J. H., Hwang, K. A., ... Chun, K. H. (2015). Galectin-3 activates PPARγ and supports white adipose tissue formation and high-fat diet-induced obesity. Endocrinology, 156(1), 147-156. https://doi.org/10.1210/en.2014-1374
Baek, Jung Hwan ; Kim, Seok Jun ; Kang, Hyeok Gu ; Lee, Hyun Woo ; Kim, Jung Hoon ; Hwang, Kyung A. ; Song, Jaewhan ; Chun, Kyung Hee. / Galectin-3 activates PPARγ and supports white adipose tissue formation and high-fat diet-induced obesity. In: Endocrinology. 2015 ; Vol. 156, No. 1. pp. 147-156.
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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.",
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Baek, JH, Kim, SJ, Kang, HG, Lee, HW, Kim, JH, Hwang, KA, Song, J & Chun, KH 2015, 'Galectin-3 activates PPARγ and supports white adipose tissue formation and high-fat diet-induced obesity', Endocrinology, vol. 156, no. 1, pp. 147-156. https://doi.org/10.1210/en.2014-1374

Galectin-3 activates PPARγ and supports white adipose tissue formation and high-fat diet-induced obesity. / Baek, Jung Hwan; Kim, Seok Jun; Kang, Hyeok Gu; Lee, Hyun Woo; Kim, Jung Hoon; Hwang, Kyung A.; Song, Jaewhan; Chun, Kyung Hee.

In: Endocrinology, Vol. 156, No. 1, 01.01.2015, p. 147-156.

Research output: Contribution to journalArticle

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T1 - Galectin-3 activates PPARγ and supports white adipose tissue formation and high-fat diet-induced obesity

AU - Baek, Jung Hwan

AU - Kim, Seok Jun

AU - Kang, Hyeok Gu

AU - Lee, Hyun Woo

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AU - Hwang, Kyung A.

AU - Song, Jaewhan

AU - Chun, Kyung Hee

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N2 - 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.

AB - 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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