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引用次数: 108

摘要

背景:有证据表明,生命早期的营养不良会导致生长迟缓,导致成年后代谢综合征的出现。然而,对肥胖的影响似乎不太明确。目的:探讨代谢综合征背景下胎儿和产后营养不良对肥胖规划的影响,以及中心性肥胖与心血管疾病的关系。方法:回顾了最近的一些论文,这些论文探讨了母体营养与胎儿生长受损以及人类和动物后来的肥胖、心血管疾病、高血压和糖尿病之间的联系机制。结果:肥胖在胎儿期和产后早期的程序取决于产妇营养不良的时间和产后环境。肥胖主要发生在妊娠早期营养不良的后代中,这些后代表现出早期的追赶性生长。这种编程可能涉及食欲控制或激素环境的失调,导致有利于肥胖发展的环境(皮质类固醇的高分泌、高胰岛素血症和高瘦素血症以及IGF轴的异常)。脂肪组织积极分泌几种与炎症、血压、凝血和纤维蛋白溶解有关的因子。因此,早期生长受限后腹内肥胖的程序化发展可能有利于高血压和心血管疾病的高患病率。结论:腹部肥胖出现在营养不良的后代中,并因早期追赶性生长而加重。生长受限后观察到腹部肥胖的高发率可能参与高血压并产生动脉粥样硬化性血栓,从而导致心血管疾病的发展。
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Programming of obesity and cardiovascular disease.

Background: There is evidence that malnutrition in early life induces a growth retardation leading, in adult life, to manifest components of the metabolic syndrome. However, the impact on obesity seems less clearly established.

Objective: To review the effects of foetal and postnatal malnutrition on the programming of obesity in the context of the metabolic syndrome, as well as the link between central obesity and cardiovascular diseases.

Methods: Included in the review were recent papers exploring the mechanisms linking maternal nutrition with impaired foetal growth and later obesity, cardiovascular disease, hypertension and diabetes in humans and animals.

Results: The programming of obesity during foetal and early postnatal life depends of the timing of maternal malnutrition as well as the postnatal environment. Obesity arises principally in offspring submitted to malnutrition during early stages of gestation and which presented early catch-up growth. The programming may involve the dysregulation of appetite control or the hormonal environment leading to a context favourable to obesity development (hypersecretion of corticosteroids, hyperinsulinaemia and hyperleptinaemia and anomalies in the IGF axis). Adipose tissue secretes actively several factors implicated in inflammation, blood pressure, coagulation and fibrinolysis. The programmed development of intra-abdominal obesity after early growth restriction may thus favour higher prevalence of hypertension and cardiovascular diseases.

Conclusions: Abdominal obesity appears in malnourished offspring and is aggravated by early catch-up growth. Higher rates of intra-abdominal obesity observed after growth restriction may participate to hypertension and create atherothrombotic conditions leading to the development of cardiovascular diseases.

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