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首页> 外文期刊>The Journal of Nutritional Biochemistry >A maternal mouse diet with moderately high-fat levels does not lead to maternal obesity but causes mesenteric adipose tissue dysfunction in male offspring
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A maternal mouse diet with moderately high-fat levels does not lead to maternal obesity but causes mesenteric adipose tissue dysfunction in male offspring

机译：高脂肪水平的母体小鼠饮食不会导致母体肥胖，但会导致雄性后代肠系膜脂肪组织功能障碍

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The impact of an increase in maternal fat consumption on fetal metabolic programming separately from maternal obesity remains unclear. The purpose of this study was to document the effect of in utero high-fat diet exposure on the development of metabolic syndrome characteristics in offspring. C57BL/6 female mice were fed either a control diet (10% fat) or a moderately high-fat (MHF) diet (45% fat) until delivery. All pups were fostered to mothers fed with the control diet. Pups were raised on the control diet and assessed until 35 weeks of age. The caloric intake from fat was significantly increased in the MHF dams compared with the control dams. There were no significant differences in the maternal weight at mating or at gestational Day 18 between the two groups. The MHF offspring did not become obese, but they developed hypertension and glucose intolerance. Moreover, the MHF offspring had significantly higher serum non-esterified fatty acid and triglyceride levels during the refeeding state following fasting as compared with the control offspring. Serum adiponectin levels were significantly lower, and the cell size of the mesenteric adipose tissue was significantly larger in the MHF offspring than in the control offspring. The mRNA levels of the proinflammatory macrophage markers in the mesenteric adipose tissue were significantly higher in the MHF offspring than those of the control offspring. These results suggest that in utero high-fat diet exposure causes hypertension and glucose intolerance resulting from mesenteric adipose tissue dysfunction in offspring, independently of maternal obesity. (C) 2015 Elsevier Inc. All rights reserved.
机译：孕产妇脂肪消耗增加对胎儿代谢程序的影响与孕产妇肥胖分开尚不清楚。这项研究的目的是证明子宫内高脂饮食暴露对后代代谢综合征特征发展的影响。给C57BL / 6雌性小鼠喂食对照饮食（10％脂肪）或中度高脂肪（MHF）饮食（45％脂肪）直至分娩。所有的幼崽都饲养在喂养对照饮食的母亲身上。在对照饮食中饲养幼崽并评估直至35周龄。与对照水坝相比，MHF水坝的脂肪热量摄入显着增加。两组之间在交配或妊娠第18天时的孕产妇体重没有显着差异。 MHF后代没有肥胖，但是他们发展为高血压和葡萄糖不耐症。此外，与对照后代相比，在禁食后的进食状态下，MHF后代的血清非酯化脂肪酸和甘油三酸酯水平明显更高。 MHF后代的血清脂联素水平明显降低，肠系膜脂肪组织的细胞大小明显大于对照后代。在MHF后代中，肠系膜脂肪组织中促炎性巨噬细胞标志物的mRNA水平显着高于对照后代。这些结果表明，在子宫内高脂饮食暴露会导致高血压和葡萄糖耐受不良，这是由后代肠系膜脂肪组织功能障碍引起的，与母体肥胖无关。 （C）2015 Elsevier Inc.保留所有权利。

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