Early origins of the metabolic syndrome: Role of small size at birth, early postnatal weight gain, and adult IGF-I

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Abstract

Background: The relationship between low birth weight and increased risk for metabolic syndrome (MetS) in later life has been frequently described, but mechanisms underlying this association remain unknown. Methods: In 280 young adults of the PROGRAM study, aged 18-24 yr, we investigated associations of birth weight, gain in weight for length during early life, and adult IGF-I SD score (SDS), with number of MetS components (ordinal regression analyses), prevalence of MetS components and MetS (logistic regression analyses), and other metabolic parameters (linear regression analyses). Revised criteria of the National Cholesterol Educational Program (Adult Treatment Panel III) were used to determine components of MetS. The other metabolic parameters were C-reactive protein, insulin sensitivity, trunk fat mass, total cholesterol, and low-density lipoprotein cholesterol. Results: More gain in weight for length SDS in the first 3 months of life was significantly associated with an increased number of MetS components [odds ratio (OR) = 1.34], prevalence of low highdensity lipoprotein cholesterol (OR = 1.49), prevalence of MetS (OR = 2.51), increased C-reactive protein levels, and lower insulin sensitivity (P = 0.007) at the age of 21 yr. Low birth weight SDS was associated with lower insulin sensitivity (P = 0.036), but low birth weight SDS and adult IGF-I SDS were not significantly associated with any of the MetS components or MetS prevalence at 21 yr. Conclusion: Our study demonstrates that higher gain in weight for length in the first 3 months of life is associated with a higher prevalence of MetS at 21 yr, whereas low birth weight and low adult IGF-I are not. Copyright © 2012 by The Endocrine Society.

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Kerkhof, G. F., Leunissen, R. W. J., & Hokken-Koelega, A. C. S. (2012). Early origins of the metabolic syndrome: Role of small size at birth, early postnatal weight gain, and adult IGF-I. Journal of Clinical Endocrinology and Metabolism, 97(8), 2637–2643. https://doi.org/10.1210/jc.2012-1426

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