Metges Cornelia C
Research Institute of Farm Animal Biology, Research unit Nutritional Physiology, Dummerstorf, Germany.
Adv Exp Med Biol. 2009;646:105-12. doi: 10.1007/978-1-4020-9173-5_11.
Epidemiological evidence suggests that in utero as well as early postnatal life exposure to an imbalanced nutrition are both related to a greater propensity to become obese in later life. Rodent and sheep models of metabolic programming of obesity by early life nutrition include maternal low and high dietary protein and energy or food intake as well as high fat diets. Maternal nutritional imbalance during pregnancy and/or lactation programs energy expenditure, food intake and physical activity in the offspring. Underlying mechanisms of altered energy balance in programmed offspring are associated with disturbances of ontogeny of hypothalamic feeding circuits, leptin and glucocorticoid action which have long-lasting effects on food intake, energy expenditure and fat tissue metabolism.
流行病学证据表明，子宫内以及出生后早期暴露于营养不均衡环境均与日后发生肥胖的更大倾向相关。通过早期营养对肥胖进行代谢编程的啮齿动物和绵羊模型包括母体低蛋白和高蛋白饮食、能量或食物摄入以及高脂肪饮食。孕期和/或哺乳期母体营养失衡会对后代的能量消耗、食物摄入和身体活动进行编程。程序化后代能量平衡改变的潜在机制与下丘脑进食回路、瘦素和糖皮质激素作用的个体发育紊乱有关，这些紊乱对食物摄入、能量消耗和脂肪组织代谢具有长期影响。
