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近年来,越来越多的证据显示低出生体重与成年期的胰岛素抵抗综合征的发生密切相关,其发生机制尚不清楚,可能的发生机制如下:(1)宫内不良环境影响关键阶段胎儿的发育,影响胎儿组织的生长和分化,使胰岛β细胞数量减少和功能减低;(2)宫内不良环境的刺激导致持续的下丘脑-垂体-肾上腺轴活动增强,此外,还可选择性地抑制胎盘11β-羟甾类脱氢酶的功能,导致内源性糖皮质激素过多进入胎儿体内;(3)可能存在某种基因基础,导致胎儿宫内发育迟缓及成年期的胰岛素抵抗,由基因决定的胰岛素抵抗减弱了胰岛素介导的胎儿生长,并引起成年的胰岛素抵抗、糖耐量减低、糖尿病和高血压。
In recent years, more and more evidences show that low birth weight is closely related to the occurrence of insulin resistance syndrome in adulthood. The mechanism is still unclear. The possible mechanisms are as follows: (1) The key stage of intrauterine adverse environmental impact Fetus , Affecting the growth and differentiation of fetal tissue, reducing the number and function of pancreatic β-cells; (2) The stimulation of the intrauterine adverse environment results in an increased activity of the hypothalamus-pituitary-adrenal axis, and optionally Inhibit placental 11β-hydroxysteroid dehydrogenase function, leading to excessive endogenous glucocorticoid into the fetus; (3) there may be some genetic basis, leading to fetal intrauterine growth retardation and adulthood of insulin resistance, from Gene-determined insulin resistance attenuates insulin-mediated fetal growth and causes adult insulin resistance, impaired glucose tolerance, diabetes and hypertension.