首页> 外文期刊>Gynecological endocrinology: the official journal of the International Society of Gynecological Endocrinology >Association between intrauterine mild hyperglycemia and post-natal high-fat diet with adiponectin and AMPK pathway genes
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Association between intrauterine mild hyperglycemia and post-natal high-fat diet with adiponectin and AMPK pathway genes

机译:宫内轻度高血糖与产后高脂饮食与脂联素和AMPK通路基因的关系

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摘要

To investigate the mechanisms of maternal-fetal interactions in the setting of gestational diabetes mellitus. We investigated the long-term effects of intrauterine mild hyperglycemia and a postnatal high-fat diet on the glucose metabolism of adult offspring, and explored the role of adiponectin on hepatic gluconeogenesis. Twenty-one pregnant Wistar rats were randomly divided into an intrauterine hyperglycemia group (group D, n = 14) and a control group (group C, n = 7). Offspring were divided into four groups according to intrauterine blood glucose level and post-weaning dietary patterns (high-fat diet groups: DF and CF or normal diet groups: DN and CN, n = 8 per group). The average birth weights of group D offspring were higher than for group C. In the DF rats, low adiponectin mRNA expression in perirenal and epididymal fat was significantly positively correlated with low hepatic AdipoR1 mRNA expression and significantly correlated with high hepatic PEPCK, G-6-Pase, and PGC-1 alpha mRNA levels. In DF rats, hepatic P-AMPK was cytoplasmically located and its level was decreased; in these rats, hepatic CRTC2 was expressed in the nucleus and its level was significantly increased. Our study shows that the dietary structure of offspring has a large influence on the incidence of abnormal glucose tolerance.
机译:调查母婴互动在妊娠糖尿病环境中的机制。我们调查了宫内轻度高血糖症和产后高脂饮食对成年后代葡萄糖代谢的长期影响,并探讨了脂联素在肝糖原异生中的作用。将二十一只怀孕的Wistar大鼠随机分为子宫内高血糖组(D组,n = 14)和对照组(C组,n = 7)。根据宫内血糖水平和断奶后饮食模式将后代分为四组(高脂饮食组:DF和CF或正常饮食组:DN和CN,每组n = 8)。 D组后代的平均出生体重高于C组。在DF大鼠中,肾周和附睾脂肪中脂联素mRNA低表达与肝AdipoR1 mRNA低表达显着正相关,并与肝PEPCK,G-6高表达显着相关-Pase和PGC-1αmRNA水平。在DF大鼠中,肝P-AMPK位于细胞质中,其水平降低。在这些大鼠中,肝CRTC2在细胞核中表达,并且其水平显着增加。我们的研究表明,后代的饮食结构对异常葡萄糖耐量的发生有很大的影响。

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