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尽管瘦素敏感,母体高脂肪饮食仍会导致后代代谢紊乱。

Maternal high-fat diet programs for metabolic disturbances in offspring despite leptin sensitivity.

机构信息

Laboratory of Morphometry, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.

出版信息

Neuroendocrinology. 2012;96(4):272-84. doi: 10.1159/000336377. Epub 2012 Mar 23.

DOI:10.1159/000336377
PMID:22456428
Abstract

A fatty diet during pregnancy in mouse dams causes metabolic abnormalities (similar to metabolic syndrome in humans) in the rodents' offspring. We tested the hypothesis that the offspring of dams fed a high-fat diet during pregnancy and lactation develop metabolic abnormalities and leptin resistance. Pregnant C57BL/6 mice (n = 20) were fed either standard chow (SC; 19% fat) or a high-fat diet (HF; 49% fat). After weaning, male offspring were divided into four groups, according to the diet of dams and offspring: SC(dams)/SC(offspring), SC/HF, HF/SC and HF/HF (n = 30/group). For a metabolic analysis, we evaluated body mass, fat mass depots, blood plasma and adipocyte structure at 12 weeks of age. To analyse leptin sensitivity, each group was divided into two groups (vehicle or leptin) to identify the feeding response and pSTAT3 expression after acute intracerebroventricular (ICV) treatment. The offspring of mothers fed a high-fat diet presented increased body mass and visceral fat, adipocyte hypertrophy and insulin resistance. This phenotype was not associated with central leptin resistance. Thus, maternal programming by HF predisposes offspring to metabolic abnormalities despite leptin sensitivity.

摘要

孕期母鼠高脂肪饮食会导致其后代出现代谢异常(类似于人类的代谢综合征)。我们检验了这样一个假设,即孕期和哺乳期经高脂肪饮食喂养的母鼠的后代会出现代谢异常和瘦素抵抗。将怀孕的 C57BL/6 小鼠(n = 20)分为两组,分别喂食标准饲料(SC;19%脂肪)或高脂肪饮食(HF;49%脂肪)。断奶后,雄性后代根据母鼠和后代的饮食情况分为四组:SC(母鼠)/SC(后代)、SC/HF、HF/SC 和 HF/HF(每组 n = 30)。为了进行代谢分析,我们在 12 周龄时评估了体重、脂肪组织、血浆和脂肪细胞结构。为了分析瘦素敏感性,每组又分为两组(载体或瘦素),以确定急性侧脑室(ICV)治疗后的摄食反应和 pSTAT3 表达。经高脂肪饮食喂养的母鼠后代体重和内脏脂肪增加,脂肪细胞肥大,胰岛素抵抗。这种表型与中枢性瘦素抵抗无关。因此,尽管瘦素敏感,但 HF 引起的母体编程会使后代易患代谢异常。

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