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膳食鱼油对蔗糖喂养的胰岛素抵抗大鼠的血浆瘦素和脂联素水平具有正向调节作用。

Dietary fish oil positively regulates plasma leptin and adiponectin levels in sucrose-fed, insulin-resistant rats.

作者信息

Rossi Andrea S, Lombardo Yolanda B, Lacorte Jean-Marc, Chicco Adriana G, Rouault Christine, Slama Gérard, Rizkalla Salwa W

机构信息

Dept. of Biochemistry, School of Biochemistry, University of Litoral, Ciudad Universitaria, Paraje El Pozo C.C 242, 3000 Santa Fe, Argentina.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2005 Aug;289(2):R486-R494. doi: 10.1152/ajpregu.00846.2004.

DOI:10.1152/ajpregu.00846.2004
PMID:16014450
Abstract

Insulin resistance and adiposity induced by a long-term sucrose-rich diet (SRD) in rats could be reversed by fish oil (FO). Regulation of plasma leptin and adiponectin levels, as well as their gene expression, by FO might be implicated in these findings. This study was designed to evaluate the long-term regulation of leptin and adiponectin by dietary FO in a dietary model of insulin resistance induced by long-term SRD in rats and to determine their impact on adiposity and insulin sensitivity. Rats were randomized to consume a control diet (CD; n = 25) or an SRD (n = 50) for 7 mo. Subsequently, the SRD-fed rats were randomized to consume SRD+FO or to continue on SRD for an additional 2 mo. Long-term SRD induced overweight and decreased both plasma leptin and adiponectin levels without change in gene expression. Dyslipidemia, adiposity, and insulin resistance accompanied these modifications. Shifting the source of fat to FO for 2 mo increased plasma levels of both adipokines, reversed insulin resistance and dyslipidemia, and improved adiposity. These results were not associated with modifications in gene expression. These results suggest that increasing both adipokines by dietary FO might play an essential role in the normalization of insulin resistance and adiposity in dietary-induced, insulin-resistant models.

摘要

长期富含蔗糖饮食(SRD)诱导的大鼠胰岛素抵抗和肥胖可被鱼油(FO)逆转。FO对血浆瘦素和脂联素水平及其基因表达的调节可能与这些发现有关。本研究旨在评估在长期SRD诱导的大鼠胰岛素抵抗饮食模型中,膳食FO对瘦素和脂联素的长期调节作用,并确定它们对肥胖和胰岛素敏感性的影响。将大鼠随机分为两组,一组食用对照饮食(CD;n = 25),另一组食用SRD(n = 50),持续7个月。随后,将食用SRD的大鼠随机分为两组,一组食用SRD + FO,另一组继续食用SRD,再持续2个月。长期SRD导致大鼠超重,血浆瘦素和脂联素水平均降低,而基因表达无变化。这些改变伴随着血脂异常、肥胖和胰岛素抵抗。将脂肪来源改为FO持续2个月可提高两种脂肪因子的血浆水平,逆转胰岛素抵抗和血脂异常,并改善肥胖。这些结果与基因表达的改变无关。这些结果表明,膳食FO增加两种脂肪因子可能在饮食诱导的胰岛素抵抗模型中胰岛素抵抗和肥胖的正常化过程中起重要作用。

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