儿童早期代谢风险:早起鸟研究。

T J Wilkin, L D Voss, B S Metcalf, K Mallam, A N Jeffery, S Alba, M J Murphy
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引用次数: 40

摘要

目的:十多年来,怀孕期间营养不良,表现为出生时体重过轻,被认为是导致以后生活中胰岛素抵抗的因素。然而,出生体重正在上升,胰岛素抵抗状态,如糖尿病,速度更快。当代社会的胰岛素抵抗需要其他的解释。本文引用了早期儿童胰岛素抵抗与代谢紊乱关系的EarlyBird研究数据。设计:EarlyBird是一项无干预前瞻性队列研究,它的问题是“哪些儿童会产生胰岛素抵抗,为什么会这样?”它的独特之处在于从年轻时连续采集血液样本,以监测胰岛素抵抗的行为及其代谢相关因素,并对已知或被认为影响胰岛素抵抗的因素进行全面评估。受试者:总共随机选择307名入学时(平均年龄4.9岁)和12个月和24个月后的健康学龄儿童。测量方法:在儿童中:出生体重和在每个时间点的身高、体重、体重指数(BMI, kg/m(2))、五个部位的皮肤褶皱、周长、静息能量消耗、体力活动、身体组成、心率变异性、饮食、HOMA-IR和HOMA-ISC、血压、全血细胞计数、血红蛋白和红细胞压积、HbA1C、总胆固醇、HDL胆固醇、LDL胆固醇、甘油三酯、尿酸、IGF-1、促性腺激素和SHBG。父母的基线身高、体重、BMI、腰围、HOMA-IR和HOMA-ISC、全血细胞计数、红细胞压积、HbA1C、总胆固醇、HDL胆固醇、计算LDL胆固醇、甘油三酯、尿酸、促性腺激素和SHBG。结果:本文报道了四个观察结果:(1)当代儿童胰岛素抵抗与5岁体重有明显的相关性,但与出生体重无关。(2)女性在一生中都比男性更具有胰岛素抵抗性。(3)幼儿体育活动的实质性变化应归因于儿童本身,而不是其环境。(4)幼儿肥胖与胰岛素抵抗之间存在分离。结论:关于儿童肥胖和胰岛素抵抗的发展还有很多需要了解的。仅仅将营养过剩和运动不足的概念过于简单化。
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Metabolic risk in early childhood: the EarlyBird Study.

Objective: For a decade or more, poor nutrition during gestation, expressed as low weight at birth, was held to be the factor responsible for insulin resistance later in life. Birth weights, however, are rising and insulin-resistant states, such as diabetes, faster still. Alternative explanations are needed for insulin resistance in contemporary society. This review cites data from the EarlyBird study on the relationships of insulin resistance and metabolic disturbance in early childhood.

Design: EarlyBird is a nonintervention prospective cohort study that asks the question 'Which children develop insulin resistance, and why?' It is unique in taking serial blood samples from a young age with which to monitor the behaviour of insulin resistance and its metabolic correlates, and in its comprehensive assessment of factors known or thought to influence insulin resistance

Subjects: In all, 307 randomly selected healthy school children at school entry (mean age 4.9 y) and at 12 and 24 months later.

Measurements: In the children: Birth weight and, at each time point height, weight, body mass index (BMI, kg/m(2)), skinfolds at five sites, circumferences, resting energy expenditure, physical activity, body composition, heart rate variability, diet, HOMA-IR and HOMA-ISC, blood pressure, full blood count, haemoglobin and haematocrit, HbA1C, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, uric acid, IGF-1, gonadotrophins and SHBG. In their parents: At baseline height, weight, BMI, waist circumference, HOMA-IR and HOMA-ISC, full blood count, haematocrit, HbA1C, total cholesterol, HDL cholesterol, calculated LDL cholesterol, triglycerides, uric acid, gonadotrophins and SHBG.

Results: Four observations are reported here: (1) There are clear correlations in contemporary children between insulin resistance and weight at 5 y, but none with birth weight. (2) Females throughout life are intrinsically more insulin resistant than males. (3) The substantial variation of physical activity among young children is attributable to the child, and not to his environment. (4) There is dissociation in young children between fatness and insulin resistance.

Conclusion: There is much yet to be learned about the development of obesity and insulin resistance in children. The notions of overnutrition and underactivity alone are too simplistic.

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Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis. Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores. Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance. Fat storage in pancreas and in insulin-sensitive tissues in pathogenesis of type 2 diabetes. Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases.
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