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Effects of Eicosapentaenoic Acid (EPA) Treatment on Insulin Sensitivity in an Animal Model of Diabetes: Improvement of the Inflammatory Status
Author(s) -
Figueras Maite,
Olivan Mireia,
Busquets Sílvia,
LópezSoriano Francisco J.,
Argilés Josep M.
Publication year - 2011
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2010.194
Subject(s) - medicine , endocrinology , eicosapentaenoic acid , adipose tissue , insulin , white adipose tissue , chemistry , lipid metabolism , insulin resistance , fatty acid , glut4 , glucose uptake , fatty acid metabolism , carbohydrate metabolism , metabolism , biochemistry , polyunsaturated fatty acid
In addition to decreased insulin sensitivity, diabetes is a pathological condition associated with increased inflammation. The ω‐3 fatty acids have been proposed as anti‐inflammatory agents. Thus, the major goal of this study was to analyze the effects of fatty acid supplementation on both insulin sensitivity and inflammatory status in an animal model of type 2 diabetes. Diabetic rats (Goto‐Kakizaki model) were treated with eicosapentaenoic acid (EPA) or linoleic acid at 0.5 g/kg body weigh (bw) dose. In vivo incorporation of 14 C‐triolein into adipose tissue was improved by the ω‐3 administration. In vitro incubations of adipose tissue slices from EPA‐treated rats showed an increase in 14 C‐palmitate incorporation into the lipid fraction. These observations were linked with a decreased rate of fatty acid oxidation. EPA treatment resulted in a decreased fatty acid oxidation in incubated strips from extensor digitorum longus (EDL) muscles. The changes in lipid utilization were associated with a decrease in insulin plasma concentration, suggesting an improvement in insulin sensitivity. These changes in lipid metabolism were associated with an activation of AMP‐activated protein kinase (AMPK) in white adipose tissue. In addition, EPA treatment resulted in a decreased content of peroxisome proliferator‐activated receptor‐α (PPARα) and PPARδ and in increased GLUT4 expression in skeletal muscle. Moreover, EPA increased 2‐deoxy‐D‐[ 14 C]glucose (2‐DOG) uptake in C2C12 myotubes, suggesting an improvement in glucose metabolism. Concerning the inflammatory status, EPA treatment resulted in a decreased gene expression for both tumor necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6) both in skeletal muscle and adipose tissue. The data suggest that EPA treatment to diabetic rats clearly improves lipid metabolism although the evidences on insulin sensitization are less clear.