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首页> 外文期刊>The Journal of Nutritional Biochemistry >Maternal supplementation with conjugated linoleic acid in the setting of diet-induced obesity normalises the inflammatory phenotype in mothers and reverses metabolic dysfunction and impaired insulin sensitivity in offspring
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Maternal supplementation with conjugated linoleic acid in the setting of diet-induced obesity normalises the inflammatory phenotype in mothers and reverses metabolic dysfunction and impaired insulin sensitivity in offspring

机译：在饮食引起的肥胖中，母亲补充共轭亚油酸可使母亲的炎症表型正常化，并逆转后代的代谢功能障碍和胰岛素敏感性受损

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摘要

Maternal consumption of a high-fat diet significantly impacts the fetal environment and predisposes offspring to obesity and metabolic dysfunction during adulthood. We examined the effects of a high-fat diet during pregnancy and lactation on metabolic and inflammatory profiles and whether maternal supplementation with the anti-inflammatory lipid conjugated linoleic acid (CLA) could have beneficial effects on mothers and offspring. Sprague-Dawley rats were fed a control (CD; 10% kcal from fat), CLA (CLA; 10% kcal from fat, 1% total fat as CLA), high-fat (HF; 45% kcal from fat) or high fat with CLA (HFCLA; 45% kcal from fat, 1% total fat as CLA) diet ad libitum 10 days prior to and throughout gestation and lactation. Dams and offspring were culled at either late gestation (fetal day 20, F20) or early postweaning (postnatal day 24, P24). CLA, HF and HFCLA dams were heavier than CD throughout gestation. Plasma concentrations of proinflammatory cytokines interleukin-1 beta and tumour necrosis factor-alpha were elevated in HF dams, with restoration in HFCLA dams. Male and female fetuses from HF dams were smaller at F20 but displayed catch-up growth and impaired insulin sensitivity at P24, which was reversed in HFCLA offspring. HFCLA dams at P24 were protected from impaired insulin sensitivity as compared to HF dams. Maternal CLA supplementation normalised inflammation associated with consumption of a high-fat diet and reversed associated programming of metabolic dysfunction in offspring. This demonstrates that there are critical windows of developmental plasticity in which the effects of an adverse early-life environment can be reversed by maternal dietary interventions. (C) 2015 Elsevier Inc. All rights reserved.
机译：孕妇食用高脂饮食会严重影响胎儿环境，并使后代在成年后容易患上肥胖症和代谢功能障碍。我们检查了妊娠和哺乳期高脂饮食对代谢和炎症状况的影响，以及母亲补充抗炎脂质共轭亚油酸（CLA）是否会对母亲和后代产生有益影响。给Sprague-Dawley大鼠喂食对照组（CD; 10％大卡脂肪），CLA（CLA; 10％大卡脂肪，1％总脂肪（CLA）），高脂（HF; 45％大卡脂肪）在妊娠和哺乳前以及整个哺乳期10天，随意饮食含CLA（HFCLA; 45％的大卡脂肪，1％的CLA脂肪）。在妊娠后期（胎儿第20天，F20）或断奶后早期（产后第24天，P24）淘汰水坝和后代。在整个妊娠期间，CLA，HF和HFCLA大坝比CD重。在HF大坝中，促炎细胞因子白介素-1β和肿瘤坏死因子-α的血浆浓度升高，而在HFCLA大坝中恢复。 F20 HF母鼠的雄性和雌性胎儿较小，但在P24表现出追赶性生长，并且胰岛素敏感性受损，这在HFCLA后代中是相反的。与HF水坝相比，P24处的HFCLA水坝免受胰岛素敏感性损害。孕妇补充CLA可使与高脂饮食有关的炎症正常化，并逆转后代代谢功能障碍的相关编程。这表明存在重要的发育可塑性窗口，通过孕妇饮食干预可以逆转不良的早期生活环境的影响。 （C）2015 Elsevier Inc.保留所有权利。

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