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蔗糖诱导的脂代谢紊乱和胰岛素抵抗大鼠脂肪细胞中瘦素储存增加和分泌改变:鱼油饮食的影响。

Increased leptin storage with altered leptin secretion from adipocytes of rats with sucrose-induced dyslipidemia and insulin resistance: effect of dietary fish oil.

机构信息

Department of Biochemistry, School of Biochemistry, University of Litoral, Ciudad Universitaria Paraje El Pozo, CC 242 (3000) Santa Fe, Argentina.

出版信息

Metabolism. 2010 Jun;59(6):787-95. doi: 10.1016/j.metabol.2009.09.025. Epub 2009 Dec 16.

Abstract

This study examined the effect of long-term feeding a high-sucrose diet (SRD) on the modulation of rat adipocyte's leptin secretion and storage. For this purpose, we analyzed (a) basal and insulin-stimulated leptin release and the role of isoproterenol and palmitate on insulin-stimulated leptin secretion, (b) the correlation between leptin and glycerol released, (c) the relationship between leptin contents and adiposity, and (d) the effect of fish oil (FO) administration on the above parameters. Wistar rats were fed an SRD for 6 months. Whereas half the animals continued with SRD up to month 8, the other half was fed an SRD in which FO partially replaced corn oil from months 6 to 8. Total leptin release was reduced both basally and under insulin stimulation in SRD-fed rats. However, the ratio of leptin released after hormone stimulation to basal leptin levels was similar in the 3 dietary groups. Isoproterenol inhibited insulin-stimulated leptin release in the 3 groups, but the percentage was lower in the SRD. Palmitic acid mimicked the effect of isoproterenol. Leptin release from adipocyte of SRD-fed rats negatively correlated with glycerol release. Leptin store increased in fat pads of SRD and positively correlated with adiposity. Fish oil reduced leptin content and fat pad hypertrophy, and normalized basal lipolysis, leptinemia, and glucose homeostasis. This suggests that enhanced lipolysis and altered insulin sensitivity could play a role in the decrease of leptin released in SRD-fed rats. This is consistent with the reversion of all the alterations after FO administration.

摘要

本研究旨在探讨长期高糖饮食(SRD)对大鼠脂肪细胞瘦素分泌和储存的调节作用。为此,我们分析了:(a)基础和胰岛素刺激的瘦素释放,以及异丙肾上腺素和棕榈酸对胰岛素刺激的瘦素分泌的作用;(b)瘦素和甘油释放之间的相关性;(c)瘦素含量与肥胖的关系;(d)鱼油(FO)给药对上述参数的影响。Wistar 大鼠喂食 SRD 长达 6 个月。其中一半动物继续喂食 SRD 直至第 8 个月,另一半动物则从第 6 个月到第 8 个月用 FO 部分替代玉米油喂食 SRD。SRD 喂养的大鼠基础和胰岛素刺激下的总瘦素释放均降低。然而,在 3 种饮食组中,激素刺激后释放的瘦素与基础瘦素水平的比值相似。异丙肾上腺素抑制了 3 组胰岛素刺激的瘦素释放,但在 SRD 组中的抑制百分比较低。棕榈酸模拟了异丙肾上腺素的作用。SRD 喂养大鼠脂肪细胞的瘦素释放与甘油释放呈负相关。SRD 大鼠脂肪垫中的瘦素储存增加,并与肥胖呈正相关。鱼油降低了瘦素含量和脂肪垫肥大,并使基础脂肪分解、瘦素血症和葡萄糖稳态正常化。这表明增强的脂肪分解和改变的胰岛素敏感性可能在 SRD 喂养大鼠瘦素释放减少中起作用。这与 FO 给药后所有改变的逆转一致。

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