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Author Notes:

Corresponding author: Shane A. Norris, san@global.co.za.

The COHORTS group designed the research.

S.A.N. and C.H.D.F. conducted the research, analyzed data, wrote the manuscript, read and approved the final manuscript, and had primary responsibility for final content.

C.O. conducted the research, analyzed data, read and approved the final manuscript, and had primary responsibility for final content.

D.G., C.W.K., L.R., N.R.L., M.R.-Z., and L.M.R. conducted the research and read and approved the final manuscript.

A.D.S. conducted the research, wrote the manuscript, and read and approved the final manuscript.

N.T. conducted the research and read and approved the final manuscript.

The authors thank the following colleagues from each site.

Pelotas Birth Cohort (Brazil): Rosangela Lima; CLHNS (the Philippines): Sororro Gultiano, Josephine Avila, Lorna Perez, and Thomas McDade; New Delhi Birth Cohort Study (India): Shanti Ghosh, I.M. Moriyama, Vinod Kapani, Rajeshwari Verma, Bhaskar Singh, Arti Mishra, K.D. Gupta, K. Belwal, Dileep Gupta, and Shikha Sinha; INTCS (Guatemala): Rafael Flores, Usha Ramakrishnan, Kathryn Yount, Ruben Grajeda, Paul Melgar, Humberto Mendez, Luis Fernando Ramirez, Jere Behrman, John Hoddinott, Agnes Quisumbing, Alexis Murphy, and John Maluccio; BTT (South Africa): John Pettifor and Noel Cameron.

No potential conflicts of interest relevant to this article were reported.

Subjects:

Research Funding:

COHORTS is supported by Wellcome Trust (U.K.) and the Bill and Melinda Gates Foundation.

Funding for the individual cohorts was as follows: INTCS (Guatemala)—U.S. National Institutes of Health and U.S. National Science Foundation; Pelotas Birth Cohort (Brazil)—Wellcome Trust; New Delhi Birth Cohort Study (India)—Indian Council of Medical Research, U.S. National Center for Health Statistics, Medical Research Council (U.K.), and British Heart Foundation; BTT (South Africa)—Wellcome Trust, Human Sciences Research Council, South African Medical Research Council, South-African Netherlands Programme on Alternative Development, Anglo American Chairman’s Fund, and University of the Witwatersrand; and CLHNS (the Philippines)—U.S. National Institutes of Health.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Endocrinology & Metabolism
  • ENDOCRINOLOGY & METABOLISM
  • IMPAIRED GLUCOSE-TOLERANCE
  • YOUNG ADULTHOOD
  • GROWTH
  • FETAL
  • PROFILE
  • ORIGINS
  • OBESITY
  • MODEL
  • LIFE

Size at Birth, Weight Gain in Infancy and Childhood, and Adult Diabetes Risk in Five Low- or Middle-Income Country Birth Cohorts

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Journal Title:

Diabetes Care

Volume:

Volume 35, Number 1

Publisher:

, Pages 72-79

Type of Work:

Article | Final Publisher PDF

Abstract:

OBJECTIVE: We examined associations of birth weight and weight gain in infancy and early childhood with type 2 diabetes (DM) risk in five cohorts from low- and middle-income countries. RESEARCH DESIGN AND METHODS: Participants were 6,511 young adults from Brazil, Guatemala, India, the Philippines, and South Africa. Exposures were weight at birth, at 24 and 48 months, and adult weight, and conditional weight gain (CWG, deviation from expected weight gain) between these ages. Outcomes were adult fasting glucose, impaired fasting glucose or DM (IFG/DM), and insulin resistance homeostasis model assessment (IR-HOMA, three cohorts). RESULTS: Birth weight was inversely associated with adult glucose and risk of IFG/DM (odds ratio 0.91[95% CI 0.84-0.99] per SD). Weight at 24 and 48 months and CWG 0-24 and 24-48 months were unrelated to glucose and IFG/DM; however, CWG 48 months-adulthood was positively related to IFG/DM (1.32 [1.22-1.43] per SD). After adjusting for adult waist circumference, birth weight, weight at 24 and 48 months and CWG 0-24 months were inversely associated with glucose and IFG/DM. Birth weight was unrelated to IR-HOMA, whereas greater CWG at 0-24 and 24-48 months and 48 months-adulthood predicted higher IR-HOMA (all P < 0.001). After adjusting for adult waist circumference, birth weight was inversely related to IR-HOMA. CONCLUSIONS: Lower birth weight and accelerated weight gain after 48 months are risk factors for adult glucose intolerance. Accelerated weight gain between 0 and 24 months did not predict glucose intolerance but did predict higher insulin resistance.

Copyright information:

© 2012 by the American Diabetes Association.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/).

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