Document Detail


Effects of eicosapentaenoic acid ethyl ester on visfatin and apelin in lean and overweight (cafeteria diet-fed) rats.
MedLine Citation:
PMID:  18755047     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous studies have demonstrated that the n-3 fatty acid EPA improves insulin resistance induced by high-fat diets. The aim of the present study was to investigate the potential role of visfatin and apelin in the insulin-sensitising effects of EPA ethyl ester. The effects of EPA on muscle and adipose GLUT mRNA, as well as on liver glucokinase (GK) and glucose-6-phosphatase (G6Pase) activity, were investigated. Male Wistar rats fed on a standard diet or a high-fat cafeteria diet were daily treated by oral administration with EPA ethyl ester (1 g/kg) for 5 weeks. A significant decrease (P < 0.01) in white adipose tissue (WAT) visfatin mRNA levels was found in the cafeteria-fed rats, which was reversed by EPA administration (P < 0.05). Moreover, a negative relationship was observed between homeostatic model assessment (HOMA) and the visfatin:total WAT ratio. In contrast, cafeteria-diet feeding caused a significant increase (P < 0.01) in apelin mRNA in visceral WAT. EPA increased (P < 0.01) apelin gene expression, and a negative relationship between HOMA index with visceral apelin mRNA and serum apelin:total WAT ratio was also observed. EPA treatment did not induce changes in skeletal muscle GLUT1, GLUT4 or insulin receptor mRNA levels. Neither liver GK and G6Pase activity nor the GK:G6Pase ratio was modified by EPA. These data suggest that somehow the insulin-sensitising effects of EPA could be related to its stimulatory action on both visfatin and apelin gene expression in visceral fat, while changes in skeletal muscle GLUT, as well as in hepatic glucose production, are not likely to be the main contributing factors in the improvement in insulin resistance induced by EPA.
Authors:
Nerea Pérez-Echarri; Patricia Pérez-Matute; Beatriz Marcos-Gómez; J Alfredo Martínez; María J Moreno-Aliaga
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-08-28
Journal Detail:
Title:  The British journal of nutrition     Volume:  101     ISSN:  1475-2662     ISO Abbreviation:  Br. J. Nutr.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-03     Completed Date:  2009-06-19     Revised Date:  2011-08-03    
Medline Journal Info:
Nlm Unique ID:  0372547     Medline TA:  Br J Nutr     Country:  England    
Other Details:
Languages:  eng     Pagination:  1059-67     Citation Subset:  IM    
Affiliation:
Department of Nutrition, Food Science, Physiology and Toxicology, University of Navarra, 31008 Pamplona, Spain.
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue, White / drug effects,  metabolism
Animals
Blood Glucose / analysis
Carrier Proteins / blood,  genetics*
Diet
Eicosapentaenoic Acid / administration & dosage,  analogs & derivatives*
Gene Expression / drug effects
Glucokinase / genetics
Glucose Transporter Type 1 / genetics,  metabolism
Glucose Transporter Type 4 / genetics,  metabolism
Glucose-6-Phosphatase / genetics
Insulin / blood
Insulin Resistance
Intra-Abdominal Fat / metabolism
Liver / drug effects,  enzymology
Male
Muscle, Skeletal / metabolism
Nicotinamide Phosphoribosyltransferase / blood,  genetics*
Overweight / metabolism*
RNA, Messenger / analysis*
Rats
Rats, Wistar
Receptor, Insulin / genetics,  metabolism
Stimulation, Chemical
Chemical
Reg. No./Substance:
0/Apln protein, rat; 0/Blood Glucose; 0/Carrier Proteins; 0/Glucose Transporter Type 1; 0/Glucose Transporter Type 4; 0/RNA, Messenger; 0/Slc2a1 protein, rat; 11061-68-0/Insulin; 1553-41-9/Eicosapentaenoic Acid; 73310-10-8/eicosapentaenoic acid ethyl ester; EC 2.4.2.12/Nicotinamide Phosphoribosyltransferase; EC 2.7.1.2/Glucokinase; EC 2.7.10.1/Receptor, Insulin; EC 3.1.3.9/Glucose-6-Phosphatase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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