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  • Cambridge University Press (CUP)  (2)
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  • Cambridge University Press (CUP)  (2)
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  • 1
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    Online Resource
    Effects of eicosapentaenoic acid ethyl ester on visfatin and apelin in lean and overweight (cafeteria diet-fed) rats
    Cambridge University Press (CUP) ; 2008
    In:  British Journal of Nutrition Vol. 101, No. 7 ( 2008-08-28), p. 1059-1067
    Details
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 101, No. 7 ( 2008-08-28), p. 1059-1067
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    URL: Article
    DOI: 10.1017/S0007114508048307
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2008
    detail.hit.zdb_id: 2016047-1
    SSG: 12
    SSG: 21
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  • 2
    Online Resource
    Online Resource
    Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-α
    Cambridge University Press (CUP) ; 2007
    In:  British Journal of Nutrition Vol. 97, No. 2 ( 2007-02), p. 389-398
    Details
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 97, No. 2 ( 2007-02), p. 389-398
    Abstract: n -3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n -3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain ( P  = 0·09), a decrease in food intake ( P   〈  0·01) and an increase in leptin production ( P   〈  0·05). EPA administration reduced retroperitoneal adipose tissue weight ( P   〈  0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression ( P   〈  0·001), and also to the increase in apoptosis ( P   〈  0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased ( P   〈  0·05) by the cafeteria diet, while EPA treatment was able to prevent ( P   〈  0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    URL: Article
    DOI: 10.1017/S0007114507207627
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2007
    detail.hit.zdb_id: 2016047-1
    SSG: 12
    SSG: 21
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
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