Pinney Sara E
Division of Endocrinology and Diabetes, The Children's Hospital of Philadelphia, Department of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.
Drug Discov Today Dis Models. 2013;10(2):e71-e77. doi: 10.1016/j.ddmod.2013.01.003.
Intrauterine growth retardation has been linked to the development of type 2 diabetes later in life and the mechanisms underlying this phenomena are unknown. Epidemiological studies in humans show a distinct link with the exposure to an intrauterine insult that results in low birth weight and the development of type 2 diabetes in adulthood. Intrauterine growth retardation can be induced in rodent models by exposing the pregnant rat to a low protein diet, total calorie restriction, high dose glucocorticoids or inducing uteroplacental insufficiency, all which result in abnormalities in glucose homeostasis in the offspring later in life. Animal models of intrauterine growth retardation allow for a better characterization of changes in glucose homeostasis and corresponding changes in gene expression that can provide insight in the mechanisms by which intrauterine growth retardation leads to type 2 diabetes.
宫内生长受限与日后发生2型糖尿病有关,而这一现象背后的机制尚不清楚。人类流行病学研究表明,其与子宫内受到损伤(导致低出生体重)以及成年后发生2型糖尿病之间存在明显联系。在啮齿动物模型中,通过给怀孕大鼠喂食低蛋白饮食、进行总热量限制、给予高剂量糖皮质激素或诱发子宫胎盘功能不全,均可诱导宫内生长受限,所有这些都会导致后代日后出现葡萄糖稳态异常。宫内生长受限的动物模型有助于更好地描述葡萄糖稳态的变化以及相应的基因表达变化,从而深入了解宫内生长受限导致2型糖尿病的机制。