Birth weight and the insulin resistance syndrome: association of low birth weight with truncal obesity and raised plasminogen activator inhibitor-1 but not with abdominal obesity or plasma lipid disturbances

Birth weight and the insulin resistance syndrome: association of low birth weight with truncal obesity and raised plasminogen activator inhibitor-1 but not with abdominal obesity or plasma lipid disturbances
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DOI:
10.1007/s001250050007
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发表时间:
2000-01-01
期刊:
影响因子:
8.2
通讯作者:
Lithell, HO
Lithell, HO
中科院分区:
医学1区
文献类型:
--
作者:
Byberg, L;McKeigue, PM;Lithell, HO

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目的/假设。为了区分与出生体重相关的生理紊乱与称为胰岛素抵抗综合征的紊乱群。在瑞典乌普萨拉进行的一项基于人群的研究中,记录了出生体重的男性在50岁时(n = 1268)进行了代谢特征分析,并在70岁时(n = 734)进行了重新研究。血压、体重指数、血糖和胰岛素浓度与出生体重相关。出生体重与肩胛下:三头肌皮褶比(躯干脂肪)、纤溶酶原激活物抑制剂-1(派-1)活性、特定胰岛素和胰岛素原样分子(校正BMI后)呈负相关(p < 0.03)。出生体重与腰围、血清甘油三酯和高密度脂蛋白胆固醇无关(p > 0.10)。胰岛素抵抗综合征定义为高血压、胰岛素抵抗和血脂异常的组合。50岁和70岁时该综合征的患病率与出生体重呈负相关,出生体重每增加1 kg,比值比分别为0.66和0.71。当综合征被定义为包括躯干肥胖或提高纤溶酶原激活物抑制剂-1,而不是血脂异常,相应的比值比分别为0.51和0.66.Conclusions/interpretation。低出生体重可预测高血压、胰岛素抵抗、躯干肥胖和高纤溶酶原激活物抑制剂-1活性,但不能预测胰岛素抵抗综合征中存在的腹部肥胖或血脂异常。与低出生体重相关的一系列紊乱是一般人群中胰岛素抵抗综合征紊乱的一个子集。生理紊乱的这一子集可能通过特定的途径相关联。
Aims/hypothesis. To distinguish the physiological disturbances related to birth weight from the cluster of disturbances called the insulin resistance syndrome.Methods. Men participating in a population-based study in Uppsala, Sweden, with recordings of birth weight, were metabolically characterised at age 50 (n = 1268) and re-investigated at age 70 (n = 734). Blood pressure, BMI, glucose and insulin concentrations are associated with birth weight in this cohort.Results. Birth weight was inversely associated (p < 0.03) with subscapular:triceps skinfold ratio (truncal fat), plasminogen activator inhibitor-1 (PAI-1) activity, specific insulin and proinsulin-like molecules when adjusted for BMI. Birth weight was not related (p > 0.10) with waist circumference, serum triglycerides or HDL cholesterol. The insulin resistance syndrome was defined as the combination of hypertension, insulin resistance and dyslipidaemia. The prevalence of this syndrome at age 50 and 70 was inversely related to birth weight with odds ratio 0.66 and 0.71, respectively, per kg increase in birth weight. When the syndrome was defined to include truncal obesity or raised plasminogen activator inhibitor-1 instead of dyslipidaemia, the corresponding odds ratios were 0.51 and 0.66, respectively.Conclusions/interpretation. Low birth weight predicts high blood pressure, insulin resistance, truncal obesity and high plasminogen activator inhibitor-1 activity but not the abdominal obesity or dyslipidaemia present in the insulin resistance syndrome. The cluster of disturbances associated with low birth weight is a subset of the disturbances that are clustered in the general population as the insulin resistance syndrome. This subset of physiological disturbances is possibly linked by a specific pathway.