title: Cyclooxygenase-2 inhibition reverts the decrease in adiponectin levels and attenuates the loss of white adipose tissue during chronic inflammation.
abstract: Chronic arthritis leads to a decrease in body weight that is associated with a decrease in skeletal muscle and white adipose tissue mass. We have observed that overactivation of cyclooxygenase-2 (COX-2) is responsible for muscle wasting in arthritic rats. The aim of this work was to study the role of COX-2 in arthritis-induced white adipose tissue mass loss. Arthritis was induced in rats by Freund's adjuvant injection, and the effect of the COX-2 inhibitor meloxicam on serum concentrations of leptin, adiponectin, insulin and glycerol, as well as on gene expression of leptin, adiponectin, hormone-sensitive lipase (HSL), fatty acid synthase (FAS), tumour necrosis factor alpha (TNF) and insulin-like growth factor I (IGF-I) in white adipose tissue were determined. Arthritis decreased adipose tissue weight, serum leptin and adiponectin as well as their mRNAs in adipose tissue. Meloxicam administration to arthritic rats increased adipose tissue weight, serum concentrations of adiponectin and its mRNA in adipose tissue, but it did not modify leptin. Arthritis decreased serum insulin and FAS and IGF-I gene expression in adipose tissue. Meloxicam administration did not modify these effects. Serum concentrations of glycerol were decreased in arthritic rats. In control rats, meloxicam administration did not modify serum glycerol or adipose tissue gene expression of HSL. However, in arthritic rats HSL gene expression in adipose tissue was decreased by meloxicam. All these data indicate that COX-2 activation plays a role in the decrease in adiponectin secreted by adipocytes and in the loss in white adipose tissue mass in arthritic rats.
authors.affiliation: Department of Physiology, Faculty of Medicine, Complutense University, Madrid, Spain.
authors.forename: Miriam
authors.initials: M
authors.lastname: Granado
authors.forename: Ana Isabel
authors.initials: AI
authors.lastname: Martín
authors.forename: Estíbaliz
authors.initials: E
authors.lastname: Castillero
authors.forename: Asunción
authors.initials: A
authors.lastname: López-Calderón
authors.forename: M A Angeles
authors.initials: MA
authors.lastname: Villanúa
mesh_terms: D052242:Adiponectin / Q000378:metabolism*; D052436:Adipose Tissue, White / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D001169:Arthritis, Experimental / Q000139:chemically induced* / Q000378:metabolism*; D001835:Body Weight / Q000187:drug effects; D002908:Chronic Disease; D051546:Cyclooxygenase 2 / Q000097:blood / Q000378:metabolism*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D000077239:Meloxicam; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013843:Thiazines / Q000494:pharmacology; D013844:Thiazoles / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D052242:Adiponectin; D016861:Cyclooxygenase Inhibitors; D012333:RNA, Messenger; D013843:Thiazines; D013844:Thiazoles; D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I; D051546:Cyclooxygenase 2; D000077239:Meloxicam