Altered gene expressions of ghrelin, PYY, and CCK in the gastrointestinal tract of the hyperphagic intrauterine growth restriction rat offspring.
Altered gene expressions of ghrelin, PYY, and CCK in the gastrointestinal tract of the hyperphagic intrauterine growth restriction rat offspring.
复制标题
食量过多的宫内生长受限大鼠后代胃肠道中 ghrelin、PYY 和 CCK 基因表达的改变。
DOI：
10.1055/s-0030-1270528
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Ohzeki,T
中科院分区：
文献类型：
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作者：
Nagata,E;Nakagawa,Y;Yamaguchi,R;Fujisawa,Y;Sano,S;Satake,E;Matsushita,R;Nakanishi,T;Liu,Y;Ohzeki,T
宫内生长受限（IUGR）与成年期代谢综合征的发生率显著增加相关。动物研究表明，IUGR的后代在出生后早期是贪食的，因此表现出肥胖。IUGR中胃肠道食物摄入调节的分子机制尚未阐明。在本研究中，我们利用IUGR大鼠模型，限制母亲的食物摄入量（正常摄入量的50%，随意; FR组）从妊娠第7天直到分娩。来自营养不良母亲的幼崽由对照母亲抚养。我们检查了食物的摄入量，并评估了生长激素释放肽，肽YY（PYY），胆囊收缩素（CCK）在男性新生儿（出生后第1天）和成年后代（年龄，7个月）的消化道的基因表达。与其母亲随意接受标准饮食的后代（CON后代）相比，FR后代从断奶时间到实验结束都是贪食的，并导致最终体重更重。与对照组相比，新生儿和成年FR后代的胃中ghrelin基因表达和血浆ghrelin水平均较高。尽管FR新生儿的胃肠道基因表达和血浆中PYY和CCK的水平升高，但FR成人的胃肠道基因表达和血浆中PYY和CCK的水平降低。我们的研究结果表明，在母体营养不良引起的IUGR后代的胃肠道食欲和食欲肠肽的基因表达的改变提供了一个潜在的机制，以解释这些后代中看到的暴食和肥胖。
Intrauterine growth restriction (IUGR) is associated with a substantially greater incidence of metabolic syndrome in adulthood. Animal studies have shown that IUGR offspring are hyperphagic during the early postnatal period and therefore exhibit obesity. The molecular mechanisms underlying food intake regulation in the gastrointestinal tract have not been clarified in IUGR. In the present study, we utilized a rat model of IUGR by restricting the food intake of the mother (50% of the normal intake, ad libitum; FR group) from day 7 of gestation until delivery. Pups from undernourished mothers were fostered by control mothers. We examined the food intake and assessed the gene expressions of ghrelin, peptide YY (PYY), and cholecystokinin (CCK) in the alimentary tract of male newborns (postnatal day1) and adult offspring (age, 7 months). Compared to the offspring whose mothers received the standard diet ad libitum (CON offspring), FR offspring were hyperphagic from the weaning time until the end of the experiment, and resulted in a heavier final weight. Both newborn and adult FR offspring had higher ghrelin gene expression in the stomach and higher ghrelin plasma levels than did the controls. Although the gastrointestinal gene expressions and plasma levels of the anorexic peptides, PYY and CCK, were elevated in the FR newborns, they decreased in the FR adults. Our findings suggest that the altered gene expressions of orexigenic and anorexigenic gut peptides in the gastrointestinal tract in the maternal undernutrition-induced IUGR offspring provide a potential mechanism to explain hyperphagia and obesity seen in these offspring.