Galectin-3 activates PPARγ and supports white adipose tissue formation and high-fat diet-induced obesity.
Endocrinology
; 156(1): 147-56, 2015 Jan.
Article
in En
| MEDLINE
| ID: mdl-25343273
ABSTRACT
Galectin-3, a ß-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 ß. 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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Dietary Fats
/
Gene Expression Regulation
/
Galectin 3
/
PPAR gamma
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Adipose Tissue, White
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Obesity
Limits:
Animals
/
Female
/
Humans
/
Male
Language:
En
Journal:
Endocrinology
Year:
2015
Type:
Article