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低 n-6:n-3PUFA 比值的饮食可预防大鼠果糖诱导的血脂异常和相关肝改变:18:3n-3 与长链 n-3PUFA 的比较。

Diets with low n-6:n-3 PUFA ratio protects rats from fructose-induced dyslipidemia and associated hepatic changes: Comparison between 18:3 n-3 and long-chain n-3 PUFA.

机构信息

Department of lipid chemistry, National Institute of Nutrition, Hyderabad, India.

Department of lipid chemistry, National Institute of Nutrition, Hyderabad, India.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 2020 Apr;155:102082. doi: 10.1016/j.plefa.2020.102082. Epub 2020 Feb 22.

DOI:10.1016/j.plefa.2020.102082
PMID:32169807
Abstract

In the present study, we investigated the impact of substituting alpha-linolenic acid (ALA) or long-chain n-3 PUFA (eicosapentaenoic acid and docosahexaenoic acid) for linoleic acid and hence decreasing n-6:n-3 PUFA ratio on high-fructose diet-induced hypertriglyceridemia and associated hepatic changes. Weanling male Wistar rats were divided into four groups and fed with starch-diet (n-6:n-3 PUFA ratio 215:1) and high-fructose diets with different n-6:n-3 PUFA ratio (215:1, 2:1 with ALA and 5:1 with long-chain n-3 PUFA) for twenty-four weeks. Substitution of linoleic acid with ALA (n-6:n-3 PUFA ratio of 2) or long-chain n-3 PUFA (n-6:n-3 PUFA ratio of 5) protected the rats from fructose-induced dyslipidemia, hepatic oxidative stress and corrected lipogenic and proinflammatory gene expression. Both ALA and long-chain n-3 PUFA supplementation also reversed the fructose-induced upregulation of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) gene, which is involved in the generation of active glucocorticoids in tissues. Although both ALA and LC n-3 PUFA prevented fructose-induced dyslipidemia to a similar extent, compared to ALA, LC n-3 PUFA is more effective in preventing hepatic oxidative stress and inflammation.

摘要

在本研究中,我们研究了用α-亚麻酸(ALA)或长链 n-3PUFA(二十碳五烯酸和二十二碳六烯酸)替代亚油酸,从而降低 n-6:n-3PUFA 比值对高果糖饮食诱导的高甘油三酯血症及相关肝变化的影响。将断乳雄性 Wistar 大鼠分为四组,分别用淀粉饮食(n-6:n-3PUFA 比值为 215:1)和不同 n-6:n-3PUFA 比值的高果糖饮食(215:1、ALA 替代的 2:1 和长链 n-3PUFA 替代的 5:1)喂养 24 周。用 ALA(n-6:n-3PUFA 比值为 2)或长链 n-3PUFA(n-6:n-3PUFA 比值为 5)替代亚油酸可保护大鼠免受果糖诱导的血脂异常、肝氧化应激,并纠正脂肪生成和促炎基因表达。ALA 和长链 n-3PUFA 的补充还逆转了果糖诱导的 11β-羟类固醇脱氢酶 1(11β-HSD1)基因的上调,该基因参与组织中活性糖皮质激素的产生。尽管 ALA 和 LC n-3PUFA 均可预防果糖诱导的血脂异常,但与 ALA 相比,LC n-3PUFA 更能有效预防肝氧化应激和炎症。

相似文献

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Diets with low n-6:n-3 PUFA ratio protects rats from fructose-induced dyslipidemia and associated hepatic changes: Comparison between 18:3 n-3 and long-chain n-3 PUFA.低 n-6:n-3PUFA 比值的饮食可预防大鼠果糖诱导的血脂异常和相关肝改变:18:3n-3 与长链 n-3PUFA 的比较。
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Long-Term Measures of Dyslipidemia, Inflammation, and Oxidative Stress in Rats Fed a High-Fat/High-Fructose Diet.高脂/高果糖饮食喂养大鼠血脂异常、炎症和氧化应激的长期指标
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Low Dietary n6/n3 Ratio Attenuates Changes in the NRF 2 Gene Expression, Lipid Peroxidation, and Inflammatory Markers Induced by Fructose Overconsumption in the Rat Abdominal Adipose Tissue.低膳食n6/n3比值可减轻果糖过度摄入诱导的大鼠腹部脂肪组织中NRF 2基因表达、脂质过氧化和炎症标志物的变化。
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