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首页> 外文期刊>The Journal of Nutritional Biochemistry >Resveratrol inhibits the deleterious effects of diet-induced obesity on thymic function.
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Resveratrol inhibits the deleterious effects of diet-induced obesity on thymic function.

机译：白藜芦醇抑制饮食引起的肥胖对胸腺功能的有害作用。

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摘要

Obesity is associated with an increased risk of infectious diseases. It has been shown to have deleterious effects on cell-mediated immunity, including reducing thymocyte numbers and altering responses of thymocytes to pathogens. In the current study, we examined the efficacy of the antiobesity phytochemical resveratrol in preventing the deleterious effects of a high-fat diet on thymic anatomy and function. Compared to C57Bl/6 male mice fed a low-fat diet, mice on a high-fat diet had a significant increase in thymic weight and lipid content, and a disrupted anatomy, including a reduction of the medullary compartment and absence of a corticomedullary junction. There were a decrease in thymic cellularity and mature T-cell output, and a disrupted T-cell maturation, as evidenced by increased double-negative and decreased single- and double-positive thymocytes. Mice that had been fed resveratrol along with a high-fat diet had a dose-dependent reversal in all these parameters. Western blots from thymi showed that obese mice had lower levels of the key stimulators of lipid metabolism, phospho-5' adenosine monophosphate-activated protein kinase and its downstream target, carnitine palmitoyl transferase-1; this was restored to normal levels in resveratrol-fed mice. Resveratrol also reversed an increase in glycerol-3-phosphate acyltransferase-1, the enzyme that catalyzes the first step in triglycerol synthesis. Taken together, these results indicate that resveratrol is a potent inhibitor of the deleterious effects of diet-induced obesity on thymic anatomy and function, and this may hold promise in preventing obesity-related deficits in cell-mediated immunity
机译：肥胖与传染病风险增加有关。已显示它对细胞介导的免疫具有有害作用，包括减少胸腺细胞数量和改变胸腺细胞对病原体的反应。在当前的研究中，我们检查了抗肥胖植物化学白藜芦醇在预防高脂饮食对胸腺解剖和功能的有害影响方面的功效。与低脂饮食的C57Bl / 6雄性小鼠相比，高脂饮食的小鼠胸腺重量和脂质含量显着增加，并且解剖结构受到破坏，包括髓腔的减少和皮质肾小管交界处的缺失。 。胸腺细胞数量减少和成熟的T细胞输出减少，T细胞成熟受到破坏，这由双阴性胸腺细胞增多和单阳性和双阳性胸腺细胞减少证明。饲喂白藜芦醇和高脂饮食的小鼠在所有这些参数上都有剂量依赖性的逆转。胸腺的Western印迹表明，肥胖小鼠的脂质代谢关键刺激因子，磷酸5'腺苷单磷酸激活的蛋白激酶及其下游靶标肉碱棕榈酰转移酶-1含量较低。在以白藜芦醇喂养的小鼠中将其恢复至正常水平。白藜芦醇还逆转了3-磷酸甘油酰基转移酶-1（一种催化甘油三酯合成第一步的酶）的增加。综上所述，这些结果表明白藜芦醇是饮食诱发的肥胖对胸腺解剖和功能的有害影响的有效抑制剂，这可能有望预防肥胖相关的细胞介导的免疫缺陷

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