, Volume 43, Issue 1, pp 54-60

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

Abstract

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. [Diabetologia (2000) 43: 54–60]

Received: 14 May 1999 and in revised form: 15 July 1999