Gestational diabetes leads to the development of diabetes in adulthood in the rat

Gestational diabetes leads to the development of diabetes in adulthood in the rat
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DOI:
10.2337/diabetes.51.5.1499
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发表时间:
2002-05-01
期刊:
影响因子:
7.7
通讯作者:
Simmons, RA
Simmons, RA
中科院分区:
医学1区
文献类型:
--
作者:
Boloker, J;Gertz, SJ;Simmons, RA

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我们已经建立了一个大鼠妊娠期糖尿病模型,以确定代谢性宫内环境的改变是否与以后生活中糖尿病的发展直接相关。在妊娠第19天在妊娠大鼠中诱导子宫胎盘功能不全。假手术动物作为对照。后代在出生时发育迟缓;然而,他们在5-7周龄时赶上了。在大约8周大的时候,他们被和正常的雄性交配。在妊娠期间,这些动物发展为进行性高血糖症和高胰岛素血症,伴有葡萄糖耐量受损和胰岛素抵抗。糖尿病母亲(IDM)的后代被指定为婴儿,出生时体重较重,并在一生中保持体重。糖尿病患者在生命早期就有胰岛素抵抗,葡萄糖稳态逐渐受损。胰岛素分泌缺陷早在5周龄时就可检测到。到26周龄时,IDM明显患有糖尿病。这些数据表明,糖尿病妊娠代谢环境的改变会导致后代葡萄糖稳态的永久性缺陷,从而导致日后患糖尿病。
We have developed a model of gestational diabetes in the rat to determine whether an altered metabolic intrauterine milieu is directly linked to the development of diabetes later in life. Uteroplacental insufficiency Is induced in the pregnant rat on day 19 of gestation. Sham-operated animals serve as controls. Offspring are growth retarded at birth; however, they catch up by 5-7 weeks of age. At similar to8 weeks of age, they are bred to normal males. During pregnancy, these animals develop progressive hyperglycemia and hyperinsulinemia accompanied by impaired glucose tolerance and insulin resistance. Offspring, designated as infants of a diabetic mother (IDMs), are heavier at birth and remain heavy throughout life. IDMs are insulin resistant very early in life, and glucose homeostasis is progressively impaired. Defects In insulin secretion are detectable as early as 5 weeks of age. By 26 weeks of age, IDMs are overtly diabetic. These data demonstrate that the altered metabolic milieu of the diabetic pregnancy causes permanent defects in glucose homeostasis in the offspring that lead to the development of diabetes later in life.