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首页> 外文期刊>European Journal of Lipid Science and Technology >Maternal high-fat diet exposure leads to insulin resistance and impacts myogenic and adipogenicgene expression in offspring rats
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Maternal high-fat diet exposure leads to insulin resistance and impacts myogenic and adipogenicgene expression in offspring rats

机译:母体高脂饮食暴露会导致胰岛素抵抗并影响后代大鼠的成肌和成脂基因表达

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摘要

To obtain information on the molecular mechanisms of insulin resistance (IR) in offspring rats due to maternal high-fat diet exposure, we investigated (i) the consequences of maternal high-fat diet consumption on offspring malprogramming that predisposes the offspring to the onset of IR during adulthood and (ii) the impact of a maternal high-fat diet on myogenic and adipogenic gene expression in muscle. Sprague-Dawley female rats were randomly divided into two groups and fed either a normal chow (NC) or a high-fat diet (HF). After breeding, the pups were divided into four groups: male offspring of HF (MOH), female offspring of HF (FOH), male offspring of NC (MON) and female offspring of NC (FON). The offspring rats were fed NC until 18 weeks after weaning. The body weight, plasma parameters, oral glucose tolerance test (OGTT) and insulin sensitivity index (ISI) of the dam and the offspring rats were measured, and nuclear and mitochondrial morphologies of skeletal muscular cells of the offspring rats were observed. The expression of myogenic and adipogenic marker genes in muscle were measured during the embryonic and foetal periods. The results indicated that maternal high-fat diet exposure led to the emergence of IR in MOH and FOH. The expression of myogenic and adipogenic genes in muscular tissues was seriously disrupted in MOH and FOH, which was revealed firstly in the present study. The consequences of maternal high-fat diet consumption on offspring malprogramming that predisposes the offspring to the onset of insulin resistance during adulthood and the possible mechanism of offspring IR, that is the impact of a maternal high-fat diet on skeletal muscle and adipose tissue gene expression, were investigated.
机译:为了获得有关由于母体高脂饮食暴露引起的后代大鼠胰岛素抵抗(IR)分子机制的信息,我们调查了(i)母体高脂饮食摄入对子代不良编程的后果,该程序不当使子代易于患上高脂血症成年期间的IR和(ii)孕妇高脂饮食对肌肉中成肌和成脂基因表达的影响。将Sprague-Dawley雌性大鼠随机分为两组,并喂以正常食物(NC)或高脂饮食(HF)。繁殖后,将幼崽分为四组:HF(MOH)的雄性后代,HF(FOH)的雌性后代,NC(MON)的雄性后代和NC(FON)的雌性后代。断奶后代给后代大鼠NC喂养。测量大坝和后代大鼠的体重,血浆参数,口服葡萄糖耐量试验(OGTT)和胰岛素敏感性指数(ISI),并观察后代大鼠骨骼肌细胞的核和线粒体形态。在胚胎期和胎儿期测量肌肉中成肌和成脂标记基因的表达。结果表明,孕妇高脂饮食暴露导致MOH和FOH中IR的出现。肌肉组织中成肌和成脂基因的表达在MOH和FOH中受到严重破坏,这是本研究首先揭示的。母体高脂饮食对后代编程失调的后果,使子代成年后容易出现胰岛素抵抗,以及后代IR的可能机制,即母体高脂饮食对骨骼肌和脂肪组织基因的影响表达,进行了调查。

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