Birth weight and the Metabolic Syndrome: thrifty phenotype or thrifty genotype?

Citation
Mp. Stern et al., Birth weight and the Metabolic Syndrome: thrifty phenotype or thrifty genotype?, DIABET M R, 16(2), 2000, pp. 88-93
Citations number
28
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
DIABETES-METABOLISM RESEARCH AND REVIEWS
ISSN journal
15207552 → ACNP
Volume
16
Issue
2
Year of publication
2000
Pages
88 - 93
Database
ISI
SICI code
1520-7552(200003/04)16:2<88:BWATMS>2.0.ZU;2-S
Abstract
Background Inverse correlations have been reported between birth weight and the Metabolic Syndrome (abdominal obesity, insulin resistance, hyperinsuli nemia, glucose intolerance, dyslipidemia, and hypertension). These correlat ions are thought to reflect primarily nutritional inadequacies during fetal and early life. We explored familial influences on these correlations. Methods Using birth weight data on 602 subjects from 65 pedigrees, we parti tioned phenotypic correlations into familial and non-familial. The former a re usually regarded as reflecting primarily genetic influences, although th ey may also reflect environmental influences that are shared by family memb ers, and the latter reflect random environmental influences. Results A consistent pattern of positive familial and inverse non-familial correlations were observed. The strongest familial correlations were betwee n birth weight and fasting insulin (r=0.58, p=0.002), leptin (r=0.48, p=0.0 21), split proinsulin (r=0.51, p=0.090), and heart rate (r=0.39, p=0.037). An inverse familial correlation was observed with HDL cholesterol (r=-0.28, p=0.018). Non-familial correlations were weaker and only two subscapular-t o-triceps skinfold ratio and fasting insulin - were statistically significa nt. Conclusion Since the familial and non-familial correlations were in opposit e directions, we attribute the former to the pleiotropic effects of genes. Specifically, we conclude that genes that increase birth weight also worsen the Metabolic Syndrome in adult life. Since the inverse correlations repor ted in the literature reflect mainly cohorts born in the early part of the 20th century, improved maternal nutrition since then may have allowed the e xpression of genetic influences in our participants, all of whom were born after 1950. Copyright (C) 2000 John Wiley & Sons, Ltd.