Division of Endocrinology, Diabetes and Metabolism, First Department of Pediatrics, University of Athens, Agia Sophia Children's Hospital, Athens, Greece.
Ann N Y Acad Sci. 2010 Sep;1205:99-105. doi: 10.1111/j.1749-6632.2010.05683.x.
According to the fetal origin of adult diseases hypothesis, the intrauterine environment through developmental plasticity may permanently influence long-term health and disease. Therefore, intrauterine growth restriction (IUGR), due either to maternal, placental, or genetic factors, may permanently alter the endocrine-metabolic status of the fetus, driving an insulin resistance state that can promote survival at the short term but that facilitates the development of type 2 diabetes mellitus and metabolic syndrome in adult life, especially when the intrauterine nutrient restriction is followed by a postnatal obesogenic environment. Furthermore, an energy-rich environment during fetal programming may also drive the development of excess abdominal fat and type 2 diabetes in later life, demonstrating that both intrauterine nutrient restriction as well as intrauterine nutrient excessive supply may predispose for the development of adult diabetes.
根据成人疾病的胎儿起源假说，宫内环境通过发育可塑性可能会永久性地影响长期健康和疾病。因此，胎儿宫内生长受限（IUGR），无论是由于母体、胎盘还是遗传因素引起，都可能永久性地改变胎儿的内分泌代谢状态，导致胰岛素抵抗状态，这种状态在短期内可以促进生存，但容易导致成年后患 2 型糖尿病和代谢综合征，尤其是当宫内营养限制后又处于肥胖的后天环境中。此外，胎儿编程过程中的高能量环境也可能导致成年后腹部脂肪过多和 2 型糖尿病的发展，这表明宫内营养限制和宫内营养过度供应都可能导致成年后糖尿病的发生。
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