Lawson Health Research Institute, St. Joseph's Health Care, London, ON, Canada.
Departments of Medicine, Physiology and Pharmacology, Western University, London, ON, Canada.
Front Endocrinol (Lausanne). 2024 Sep 23;15:1456629. doi: 10.3389/fendo.2024.1456629. eCollection 2024.
Fetal and neonatal development is a critical period for the establishment of the future metabolic health and disease risk of an individual. Both maternal undernutrition and overnutrition can result in abnormal fetal organ development resulting in inappropriate birth size, child and adult obesity, and increased risk of Type 2 diabetes and cardiovascular diseases. Inappropriate adaptive changes to the maternal pancreas, placental function, and the development of the fetal pancreas in response to nutritional stress during pregnancy are major contributors to a risk trajectory in the offspring. This interconnected maternal-placental-fetal metabolic axis is driven by endocrine signals in response to the availability of nutritional metabolites and can result in cellular stress and premature aging in fetal tissues and the inappropriate expression of key genes involved in metabolic control as a result of long-lasting epigenetic changes. Such changes result is insufficient pancreatic beta-cell mass and function, reduced insulin sensitivity in target tissues such as liver and white adipose and altered development of hypothalamic satiety centres and in basal glucocorticoid levels. Whilst interventions in the obese mother such as dieting and increased exercise, or treatment with insulin or metformin in mothers who develop gestational diabetes, can improve metabolic control and reduce the risk of a large-for-gestational age infant, their effectiveness in changing the adverse metabolic trajectory in the child is as yet unclear.
胎儿和新生儿的发育是个体未来代谢健康和疾病风险建立的关键时期。母体营养不足和营养过剩都可能导致胎儿器官发育异常,导致出生体重不当、儿童和成人肥胖以及 2 型糖尿病和心血管疾病风险增加。母体胰腺、胎盘功能以及胎儿胰腺对妊娠期间营养压力的适应性变化不适当,是后代风险轨迹的主要原因。这种相互关联的母体-胎盘-胎儿代谢轴是由内分泌信号驱动的,以响应营养代谢物的可用性,可导致胎儿组织中的细胞应激和过早衰老,以及参与代谢控制的关键基因的异常表达,这是由于持久的表观遗传变化。这些变化导致胰腺β细胞数量和功能不足、肝脏和白色脂肪等靶组织的胰岛素敏感性降低,以及下丘脑饱腹感中心和基础糖皮质激素水平的发育改变。虽然对肥胖母亲进行干预,如节食和增加运动,或对患有妊娠糖尿病的母亲使用胰岛素或二甲双胍治疗,可以改善代谢控制并降低巨大儿的风险,但它们在改变儿童不良代谢轨迹方面的有效性尚不清楚。