Tags

Type your tag names separated by a space and hit enter

Effects of eicosapentaenoic acid (EPA) treatment on insulin sensitivity in an animal model of diabetes: improvement of the inflammatory status.
Obesity (Silver Spring). 2011 Feb; 19(2):362-9.O

Abstract

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.

Authors+Show Affiliations

Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20885391

Citation

Figueras, Maite, et al. "Effects of Eicosapentaenoic Acid (EPA) Treatment On Insulin Sensitivity in an Animal Model of Diabetes: Improvement of the Inflammatory Status." Obesity (Silver Spring, Md.), vol. 19, no. 2, 2011, pp. 362-9.
Figueras M, Olivan M, Busquets S, et al. Effects of eicosapentaenoic acid (EPA) treatment on insulin sensitivity in an animal model of diabetes: improvement of the inflammatory status. Obesity (Silver Spring). 2011;19(2):362-9.
Figueras, M., Olivan, M., Busquets, S., López-Soriano, F. J., & Argilés, J. M. (2011). Effects of eicosapentaenoic acid (EPA) treatment on insulin sensitivity in an animal model of diabetes: improvement of the inflammatory status. Obesity (Silver Spring, Md.), 19(2), 362-9. https://doi.org/10.1038/oby.2010.194
Figueras M, et al. Effects of Eicosapentaenoic Acid (EPA) Treatment On Insulin Sensitivity in an Animal Model of Diabetes: Improvement of the Inflammatory Status. Obesity (Silver Spring). 2011;19(2):362-9. PubMed PMID: 20885391.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of eicosapentaenoic acid (EPA) treatment on insulin sensitivity in an animal model of diabetes: improvement of the inflammatory status. AU - Figueras,Maite, AU - Olivan,Mireia, AU - Busquets,Sílvia, AU - López-Soriano,Francisco J, AU - Argilés,Josep M, Y1 - 2010/09/30/ PY - 2010/10/2/entrez PY - 2010/10/5/pubmed PY - 2011/4/30/medline SP - 362 EP - 9 JF - Obesity (Silver Spring, Md.) JO - Obesity (Silver Spring) VL - 19 IS - 2 N2 - 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. SN - 1930-739X UR - https://www.unboundmedicine.com/medline/citation/20885391/Effects_of_eicosapentaenoic_acid__EPA__treatment_on_insulin_sensitivity_in_an_animal_model_of_diabetes:_improvement_of_the_inflammatory_status_ L2 - https://doi.org/10.1038/oby.2010.194 DB - PRIME DP - Unbound Medicine ER -