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首页> 外文期刊>Journal of applied toxicology >In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin modulates dysregulation of the lipid metabolism in mouse offspring fed a high-calorie diet
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In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin modulates dysregulation of the lipid metabolism in mouse offspring fed a high-calorie diet

机译：在宫内和哺乳期暴露于2,3,7,8-四氯二苯并-对-二恶英可调节高热量饮食喂养的小鼠后代脂质代谢的失调

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Exposure to environmental chemicals, including dioxins, is a risk factor for type 2 diabetes mellitus in humans. This study explored the hypothesis that in utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most toxic congener among dioxins, aggravates this disease state later in adulthood. Pregnant C57Bl/6J mice were administered either a single oral dose of TCDD (3.0μgkg-1 body weight) or corn oil on gestational day 12.5. The male pups born to these two groups of dams were given either a regular diet or a high-calorie diet, after postnatal day (PND) 28. The four groups of investigated offspring were thus termed T-R (TCDD regular diet), T-H (TCDD high-calorie diet), V-R (vehicle regular diet), and V-H (vehicle high-calorie diet). The mice were regularly monitored for body weight, blood pressure and glucose, until they reached 26weeks of age. Mice in the V-H group were significantly obese at weeks 15 and 26, but they exhibited no diabetes-associated signs of insulin resistance or hypertension. However, metabolic syndrome-related alterations with marginal signs of liver damage were found at week 26. Pronounced signs of dysregulated lipid metabolism with altered gene expression and liver inflammation were already present at week 15, whereas such alterations were suppressed in the T-H group. Although the mechanism is unclear, this study showed that in utero and lactational exposure to low-dose TCDD does not aggravate obesity-induced disease states, such as adult-onset diabetes, but instead attenuates the dysregulation of lipid metabolism brought on by a high-calorie diet.
机译：接触环境化学物质（包括二恶英）是人类2型糖尿病的危险因素。这项研究探索了一种假设，即子宫和哺乳期暴露于二恶英中毒性最高的同类物2,3,7,8-四氯二苯并-p-二恶英（TCDD），会在成年后期加剧这种疾病。在妊娠第12.5天，给怀孕的C57Bl / 6J小鼠单次口服TCDD（3.0μgkg-1体重）或玉米油。在产后一天（PND）28之后，对这两组母坝所生的幼崽进行常规饮食或高热量饮食。因此，将四组被调查的后代称为TR（TCDD常规饮食），TH（TCDD）高热量饮食），VR（常规饮食）和VH（高热量饮食）。定期监测小鼠的体重，血压和葡萄糖，直至达到26周龄。 V-H组的小鼠在第15周和第26周显着肥胖，但未表现出与糖尿病相关的胰岛素抵抗或高血压迹象。但是，在第26周时发现了与代谢综合征相关的改变，并伴有肝损害的边缘征兆。在第15周时，已经出现了明显的脂质代谢失调，基因表达改变和肝脏炎症的征兆，而在T-H组中这种改变被抑制了。尽管机理尚不清楚，但这项研究表明，在子宫内和哺乳期接触低剂量TCDD不会加剧由肥胖引起的疾病状态，例如成年糖尿病，但可以减轻高胆固醇血症引起的脂质代谢失调。卡路里饮食。

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