Overconsumption of energy-rich foods that disrupt caloric balance is a fundamental cause of overweight, obesity and diabetes. Dysglycemia and the resulting cardiovascular disease cause substantial morbidity and mortality worldwide, as well as high societal cost. The prevalence of obesity in childhood and adolescence is increasing, leading to younger diabetes diagnosis, and higher severity of microvascular and macrovascular complications. An important goal is to identify early life conditions that increase future metabolic risk, toward the goal of preventing diabetes and cardiovascular disease. An ample body of evidence implicates prenatal and postnatal childhood growth trajectories in the programming of adult metabolic disease. Human epidemiological data show that accelerated childhood growth increases risk of type 2 diabetes in adulthood. Type 2 diabetes results from the combination of insulin resistance and pancreatic β-cell failure, but specific mechanisms by which accelerated postnatal growth impact one or both of these processes remain uncertain. This review explores the metabolic impact of overnutrition during postnatal life in humans and in rodent models, with specific attention to the connection between accelerated childhood growth and future adiposity, insulin resistance, β-cell mass and β-cell dysfunction. With improved knowledge in this area, we might one day be able to modulate nutrition and growth in the critical postnatal window to maximize lifelong metabolic health.

中文翻译：

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产后早期营养过剩会影响终生代谢风险：对胰腺 β 细胞质量和功能影响的证据

过度食用富含能量的食物会破坏热量平衡，是导致超重、肥胖和糖尿病的根本原因。血糖异常和由此产生的心血管疾病在全世界范围内导致大量发病率和死亡率，以及高昂的社会成本。儿童和青少年肥胖的患病率不断增加，导致糖尿病诊断更年轻，微血管和大血管并发症的严重程度更高。一个重要的目标是识别会增加未来代谢风险的早期生命状况，以实现预防糖尿病和心血管疾病的目标。大量证据表明，产前和产后的儿童生长轨迹与成人代谢疾病的发生有关。人类流行病学数据表明，儿童期生长加速会增加成年后患 2 型糖尿病的风险。2 型糖尿病是由胰岛素抵抗和胰腺 β 细胞衰竭共同导致的，但加速出生后生长影响其中一个或两个过程的具体机制仍不确定。本综述探讨了人类和啮齿动物模型出生后营养过剩对代谢的影响，特别关注儿童期加速生长与未来肥胖、胰岛素抵抗、β 细胞质量和 β 细胞功能障碍之间的联系。随着这一领域知识的提高，我们也许有一天能够在关键的产后窗口期调节营养和生长，以最大限度地提高终生代谢健康。