肥胖及其相关代谢性疾病与高脂饮食(high-fat diet,HFD)诱导的慢性炎症、氧化应激及肠道功能障碍密切相关。以α-亚麻酸(α-linolenic acid,ALA)、共轭亚油酸(conjugated linoleic acid,CLA)、油酸(oleic acid,OA)为主要研究对象,系统评估其对HFD诱导的肥胖小鼠代谢紊乱的干预效果。采用高脂喂养的C57BL/6 J小鼠模型,分为对照组、HFD模型组、二十碳五烯酸(eicosapentaenoic acid,EPA)阳性对照组及ALA、CLA、OA干预组(每组n=8),干预4周后分析体重、脂质水平、肠道形态及炎症和氧化应激水平。结果显示,ALA与EPA显著抑制体重增长,降低血清及肝脏的总胆固醇、甘油三酯、低密度脂蛋白胆固醇水平,上调高密度脂蛋白胆固醇水平;两者也逆转了HFD诱导的肠道绒毛缩短,增加绒隐比,抑制小肠炎症因子肿瘤坏死因子-α与白细胞介素-1β的表达,并改善小肠氧化应激(谷胱甘肽含量和超氧化物歧化酶、过氧化氢酶活性升高,丙二醛含量下降)。而CLA与OA干预则无显著调控作用。该研究表明ALA具有抗肥胖及小肠保护作用,为膳食脂质在代谢综合征中的精准调控提供了依据。
Obesity and its associated metabolic disorders are closely linked to chronic inflammation, oxidative stress, and intestinal dysfunction induced by high-fat diet (HFD).Systematically evaluated the intervention effects of α-linolenic acid (ALA), conjugated linoleic acid (CLA), and oleic acid (OA) on HFD-induced metabolic disorders in obese mice.C57BL/6 J mouse model was established with a high-fat diet and divided into the following groups, including control group (Con), HFD group, eicosapentaenoic acid (EPA) positive control group, and ALA, CLA, or OA intervention groups (n=8 per group).After 4 weeks of intervention, the weight, lipid levels, intestinal tissue morphology, and levels of inflammation and oxidative stress in mice were analyzed.The results indicated that both ALA and EPA significantly inhibited weight gain, reduced the serum and liver TC, TG, and LDL-C levels and increased the HDL-C levels.Furthermore, these fatty acids reversed the shortening of intestinal villi caused by HFD, increased the villus-crypt ratio, inhibited the expression of small intestinal inflammatory factors TNF-α and IL-1β, and improved the oxidative stress by increasing superoxide dismutase, glutathione, and catalase activities while decreasing malondialdehyde content.In contrast, interventions with CLA or OA had no significant regulatory effect.The study demonstrated that ALA had anti-obesity properties along with protective effects on the small intestine.These findings provide a foundation for precise dietary lipid regulation in addressing metabolic syndrome.
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