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首页> 美国卫生研究院文献>PLoS Clinical Trials >Postnatal Pancreatic Islet β Cell Function and Insulin Sensitivity at Different Stages of Lifetime in Rats Born with Intrauterine Growth Retardation
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Postnatal Pancreatic Islet β Cell Function and Insulin Sensitivity at Different Stages of Lifetime in Rats Born with Intrauterine Growth Retardation

机译：宫内发育迟缓大鼠出生后不同阶段的产后胰岛β细胞功能和胰岛素敏感性

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Epidemiological studies have linked intrauterine growth retardation (IUGR) to the metabolic diseases, consisting of insulin resistance, type 2 diabetes, obesity and coronary artery disease, during adult life. To determine the internal relationship between IUGR and islet β cell function and insulin sensitivity, we established the IUGR model by maternal nutrition restriction during mid- to late-gestation. Glucose tolerance test and insulin tolerance test(ITT) in vivo and glucose stimulated insulin secretion(GSIS) test in vitro were performed at different stages in IUGR and normal groups. Body weight, pancreas weight and pancreas/body weight of IUGR rats were much lower than those in normal group before 3 weeks of age. While the growth of IUGR rats accelerated after 3 weeks, pancreas weight and pancreas/body weight remained lower till 15 weeks of age. In the newborns, the fasting glucose and insulin levels of IUGR rats were both lower than those of controls, whereas glucose levels at 120 and 180 min after glucose load were significantly higher in IUGR group. Between 3 and 15 weeks of age, both the fasting glucose and insulin levels were elevated and the glucose tolerance was impaired with time in IUGR rats. At age 15 weeks, the area under curve of insulin(AUCi) after glucose load in IUGR rats elevated markedly. Meanwhile, the stimulating index of islets in IUGR group during GSIS test at age 15 weeks was significantly lower than that of controls. ITT showed no significant difference in two groups before 7 weeks of age. However, in 15-week-old IUGR rats, there was a markedly blunted glycemic response to insulin load compared with normal group. These findings demonstrate that IUGR rats had both impaired pancreatic development and deteriorated glucose tolerance and insulin sensitivity, which would be the internal causes why they were prone to develop type 2 diabetes.
机译：流行病学研究已将宫内发育迟缓（IUGR）与成年期的代谢疾病相关，包括胰岛素抵抗，2型糖尿病，肥胖症和冠状动脉疾病。为了确定IUGR与胰岛β细胞功能和胰岛素敏感性之间的内在联系，我们通过孕中期至孕期的母亲营养限制建立了IUGR模型。在IUGR和正常组的不同阶段进行体内葡萄糖耐量测试和胰岛素耐量测试（ITT）以及体外葡萄糖刺激的胰岛素分泌（GSIS）测试。 3周龄之前，IUGR大鼠的体重，胰腺重量和胰腺/体重均低于正常组。虽然IUGR大鼠的生长在3周后加速，但胰腺重量和胰腺/体重在15周龄之前仍然较低。在新生儿中，IUGR大鼠的空腹血糖和胰岛素水平均低于对照组，而IUGR组在葡萄糖负荷后120和180分钟时的血糖水平显着较高。在3至15周龄之间，IUGR大鼠的空腹血糖和胰岛素水平均升高，并且葡萄糖耐量随时间而受损。 15周龄时，IUGR大鼠葡萄糖负荷后胰岛素曲线下面积（AUCi）明显升高。同时，在15周龄的GSIS试验中，IUGR组的胰岛刺激指数明显低于对照组。 ITT在7周龄前的两组中无显着差异。然而，与正常组相比，在15周大的IUGR大鼠中，对胰岛素负荷的血糖反应明显减弱。这些发现表明，IUGR大鼠既有胰腺发育受损，又有葡萄糖耐量和胰岛素敏感性下降，这可能是它们易患2型糖尿病的内在原因。

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