Galectin-3 inhibition prevents adipose tissue remodelling in obesity.
Fiche publication
Date publication
juin 2016
Journal
International journal of obesity (2005)
Auteurs
Membres identifiés du Cancéropôle Est :
Pr ROSSIGNOL Patrick
Tous les auteurs :
Martínez-Martínez E, Calvier L, Rossignol P, Rousseau E, Fernández-Celis A, Jurado-López R, Laville M, Cachofeiro V, López-Andrés N
Lien Pubmed
Résumé
Extracellular matrix remodelling of the adipose tissue has a pivotal role in the pathophysiology of obesity. Galectin-3 (Gal-3) is increased in obesity and mediates inflammation and fibrosis in the cardiovascular system. However, the effects of Gal-3 on adipose tissue remodelling associated with obesity remain unclear. Male Wistar rats were fed either a high-fat diet (33.5% fat) or a standard diet (3.5% fat) for 6 weeks. Half of the animals of each group were treated with the pharmacological inhibitor of Gal-3, modified citrus pectin (MCP; 100 mg kg(-1) per day) in the drinking water. In adipose tissue, obese animals presented an increase in Gal-3 levels that were accompanied by an increase in pericellular collagen. Obese rats exhibited higher adipose tissue inflammation, as well as enhanced differentiation degree of the adipocytes. Treatment with MCP prevented all the above effects. In mature 3T3-L1 adipocytes, Gal-3 (10(-8 )m) treatment increased fibrosis, inflammatory and differentiation markers. In conclusion, Gal-3 emerges as a potential therapeutic target in adipose tissue remodelling associated with obesity and could have an important role in the development of metabolic alterations associated with obesity.
Mots clés
3T3-L1 Cells, Adipocytes, drug effects, Adipose Tissue, drug effects, Adiposity, drug effects, Animals, Disease Models, Animal, Galectin 3, antagonists & inhibitors, Inflammation, Male, Mice, Pectins, pharmacology, Rats, Rats, Wistar
Référence
Int J Obes (Lond). 2016 06;40(6):1034-8