Division of Endocrinology & Metabolism, National Institute of Nutrition, Hyderabad, India.
Indian J Med Res. 2009 Nov;130(5):655-65.
Epidemiological evidence indicates that poor early growth is associated with increased susceptibility to visceral obesity, insulin resistance and associated diseases in adulthood. Studies in experimental animals have demonstrated a robust association between nutrient imbalance during foetal life and disease prevalence in their later life specially of those involving macronutrient metabolism. There is very little data on the role of maternal micronutrient deficiencies widely prevalent in India. This review focuses on different animal models of micronutrient restriction, mimicking human situations during pregnancy and lactation that cause aberrations in macronutrient metabolism in the offspring. These aberrations consist of altered body composition, dyslipidaemia and altered insulin sensitivity associated with modulated insulin production. These phenotypic changes were associated with altered lipid profile, fatty acid synthesis / transport, oxidative stress, glucose tolerance / tissue uptake. Further, these were also associated with altered myogenesis and insulin expression and secretion from pancreatic beta-islets. While these changes during in utero or early postnatal life serve as essential adaptations to overcome adverse conditions, these become maladaptive subsequently and set the stage for obesity and type 2 diabetes.
流行病学证据表明，早期生长不良与成年后患内脏肥胖、胰岛素抵抗和相关疾病的易感性增加有关。实验动物研究表明，胎儿期营养失衡与它们晚年特别是涉及宏量营养素代谢的疾病患病率之间存在着很强的关联。关于在印度广泛存在的母体微量营养素缺乏在其中所起的作用，数据很少。这篇综述重点介绍了不同的微量营养素限制动物模型，模拟了妊娠和哺乳期期间的人类情况，这些情况导致后代的宏量营养素代谢异常。这些异常包括改变身体成分、血脂异常和改变胰岛素敏感性，同时伴随着胰岛素分泌的调节。这些表型变化与改变的脂质谱、脂肪酸合成/转运、氧化应激、葡萄糖耐量/组织摄取有关。此外，这些变化还与肌肉生成和胰腺β细胞的胰岛素表达和分泌的改变有关。虽然这些在子宫内或出生后早期的变化是为了克服不利条件而进行的必要适应，但随后这些变化变得不适应，并为肥胖和 2 型糖尿病奠定了基础。
