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Comparison of the effects of the n-3 polyunsaturated fatty acid eicosapentaenoic and fenofibrate on the inhibitory effect of arthritis on IGF1.

Authors
  • Castillero, Estíbaliz1
  • López-Menduiña, María
  • Martín, Ana Isabel
  • Villanúa, María Ángeles
  • López-Calderón, Asunción
  • 1 Department of Physiology, Faculty of Medicine, Complutense University of Madrid, Madrid, Spain. , (Spain)
Type
Published Article
Journal
Journal of Endocrinology
Publisher
Bioscientifica
Publication Date
Sep 01, 2011
Volume
210
Issue
3
Pages
361–368
Identifiers
DOI: 10.1530/JOE-11-0170
PMID: 21715432
Source
Medline
License
Unknown

Abstract

Adjuvant-induced arthritis is a chronic inflammatory illness that induces muscle wasting and decreases circulating IGF1. Eicosapentaenoic acid (EPA) and fenofibrate, a peroxisome proliferator-activated receptors α agonist, have anti-inflammatory actions and ameliorate muscle wasting in arthritic rats. The aim of this work was to elucidate whether EPA and fenofibrate administration are able to prevent the effect of arthritis on the IGF1-IGFBP system. On day 4 after adjuvant injection control, arthritic rats were gavaged with EPA (1 g/kg) or fenofibrate (300 mg/kg) until day 15 when all rats were killed. Arthritis decreased body weight gain, serum IGF1, and liver Igf1 mRNA, whereas it increased gastrocnemius Igfbp3 mRNA. EPA, but not fenofibrate, administration prevented arthritis-induced decrease in serum IGF1 and liver Igf1 mRNA. In the rats treated with EPA arthritis increased Igfbp5 mRNA in the gastrocnemius. Fenofibrate treatment decreased IGF1 and Igf1 mRNA in the liver and gastrocnemius. In arthritic rats, fenofibrate increased body weight gain and decreased gastrocnemius Igfbp3 and Igfbp5 mRNA. These data suggest that the mechanisms through which EPA and fenofibrate act on the IGF1 system and ameliorate muscle wasting in arthritic rats are different. EPA administration increased circulating levels of IGF1, whereas fenofibrate decreased the Igfbp3 and Igfbp5 in the gastrocnemius muscle.

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