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Body Size at Birth and Risk of Type 2 Diabetes in Adult Life

  • Yiqing Song
  • Lu Wang
  • Edwina Yeung
  • Cuilin Zhang
Chapter

Abstract

A large body of evidence supports the hypothesis that the risk of developing chronic diseases including type 2 diabetes (T2D) in adulthood is related to body size at birth. Birth weight may reflect fetal adaptation to an adverse intrauterine environment due to both genetic and environmental factors. Epidemiologic studies, primarily from prospective cohorts, have consistently shown that birth weight in the 2,500–4,000 g range is inversely associated with T2D risk in adulthood, while increased risk has been found at both extremes of low (< 2,500g) and high (> 4,000g) birth weight. The association between birth weight and risk of T2D can be modified by postnatal growth. Recent evidence appears to support that low birth weight may be related to rapid postnatal weight gain, which has been associated with increased risk for central obesity and T2D in adult life. Several mechanisms have been proposed to explain the robust association between birth weight and T2D. The “fetal origins hypothesis” remains the most popular one and has been revised based on recent evidence. This review aims to summarize both epidemiological and experimental observations relating birth weight and rapid postnatal weight gain to T2D risk in adulthood. This article will also highlight recent evidence on the mechanisms of fetal programming of diabetes due to maternal and fetal genetic factors as well as fetal epigenetic changes.

Keywords

Birth Weight High Birth Weight Fetal Programming Rapid Weight Gain Adiposity Rebound 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Abbreviations

ACE

Angiotensin-converting enzyme

BMI

Body mass index

CDKAL1

Cyclin-dependent kinase 5 regulatory subunit associated protein 1-like 1

CDKN2A/CDKN2B

Cyclin-dependent kinase inhibitor 2A/2B

CI

Confidence interval

CVD

Cardiovascular disease

FTO

Fat mass and obesity-associated gene

GCK

Glucokinase gene

GWAS

Genome-wide association studies

H19

Adult skeletal muscle gene

HFE

Human hemochromatosis gene

HHEX/IDE

Hematopoietically expressed homeobox/insulin-degrading enzyme

HPA

Hypothalamic-pituitary-adrenal axis

IGF

Insulin-like growth factor

IGF-I

Insulin-like growth factor-I

IGFR1

Insulin-like growth factor type 1 receptor

INS

Insulin gene

IUGR

Intrauterine growth restriction

JAZF1

Juxtaposed with another zinc finger gene 1

KCNJ11

Potassium inwardly-rectifying channel protein gene, subfamily 1, member 11

MC4R

Melanocortin 4 receptor

OR

Odds ratio

Pdx1

Pancreatic and duodenal homeobox 1

PPARG

Peroxisome proliferator-activated receptor gamma gene

RR

Relative risk

SGA

Small for gestational age

TCF7L2

Transcription factor 7-like 2 gene

T2D

Type 2 diabetes mellitus

UK

United Kingdom

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Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  1. 1.Division of Preventive MedicineBrigham and Women’s Hospital, Harvard Medical SchoolBostonUSA
  2. 2.Epidemiology Branch, Division of Epidemiology, Statistics, and Prevention ResearchEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of HealthBethesdaUSA

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