Skip to main content
Log in

Early life programming and metabolic syndrome

  • Prospective
  • Published:
World Journal of Pediatrics Aims and scope Submit manuscript

Abstract

Metabolic syndrome (MS) has reached epidemic proportions worldwide among children. Early life “programming” is now thought to be important in the etiology of obesity, type 2 diabetes, cardiovascular disease and MS. Nutritional imbalance and exposures to endocrine disruptor chemicals during development can increase risk for MS later in life. Epigenetic marks may be reprogrammed in response to both stochastic and environmental stimuli, such as changes in diet and the in utero environment, therefore, determination of targets for early life effects on epigenetic gene regulation provides insight into the molecular mechanisms involved in the epigenetic transgenerational inheritance of a variety of adult onset disease phenotypes. The perinatal period is a crucial time of growth, development and physiological changes in mother and child, which provides a window of opportunity for early intervention that may induce beneficial physiological alternations.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Friend A, Craig L, Turner S. The prevalence of metabolic syndrome in children: a systematic review of the literature. Metab Syndr Relat Disord 2012 Dec 18. [Epub ahead of print]

  2. Barouki R, Gluckman PD, Grandjean P, Hanson M, Heindel JJ. Developmental origins of non-communicable disease: implications for research and public health. Environ Health 2012;11:42.

    Article  PubMed  Google Scholar 

  3. Barker DJ. The origins of the developmental origins theory. J Intern Med 2007;261:412–417.

    Article  PubMed  CAS  Google Scholar 

  4. Zheng X, Wang Y, Ren W, Luo R, Zhang S, Zhang JH, et al. Risk of metabolic syndrome in adults exposed to the great Chinese famine during the fetal life and early childhood. Eur J Clin Nutr 2012;66:231–236.

    Article  PubMed  CAS  Google Scholar 

  5. Fall CH. Fetal programming and the risk of noncommunicable disease. Indian J Pediatr 2012 Jul 25.

  6. Sun B, Purcell RH, Terrillion CE, Yan J, Moran TH, Tamashiro KL. Maternal high-fat diet during gestation or suckling differentially affects offspring leptin sensitivity and obesity. Diabetes 2012;61:2833–2841.

    Article  PubMed  CAS  Google Scholar 

  7. De Coster S, van Larebeke N. Endocrine-disrupting chemicals: associated disorders and mechanisms of action. J Environ Public Health 2012;2012:713696.

    PubMed  Google Scholar 

  8. Uzumcu M, Zama AM, Oruc E. Epigenetic mechanisms in the actions of endocrine-disrupting chemicals: gonadal effects and role in female reproduction. Reprod Domest Anim 2012;47 Suppl 4:338–347.

    Article  Google Scholar 

  9. Heindel JJ, vom Saal FS. Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity. Mol Cell Endocrinol 2009;304:90–96.

    Article  PubMed  CAS  Google Scholar 

  10. Hanson M, Godfrey KM, Lillycrop KA, Burdge GC, Gluckman PD. Developmental plasticity and developmental origins of noncommunicable disease: theoretical considerations and epigenetic mechanisms. Prog Biophys Mol Biol 2011;106:272–280.

    Article  PubMed  Google Scholar 

  11. Sandovici I, Smith NH, Nitert MD, Ackers-Johnson M, Uribe-Lewis S, Ito Y, et al. Maternal diet and aging alter the epigenetic control of a promoter-enhancer interaction at the Hnf4a gene in rat pancreatic islets. Proc Natl Acad Sci U S A 2011;108:5449–5454.

    Article  PubMed  CAS  Google Scholar 

  12. Godfrey KM, Sheppard A, Gluckman PD, Lillycrop KA, Burdge GC, McLean C, et al. Epigenetic gene promoter methylation at birth is associated with child’s later adiposity. Diabetes 2011;60:1528–1534.

    Article  PubMed  CAS  Google Scholar 

  13. Skinner MK, Mohan M, Haque MM, Zhang B, Savenkova MI. Epigenetic transgenerational inheritance of somatic transcriptomes and epigenetic control regions. Genome Biol 2012;13:R91.

    Article  PubMed  CAS  Google Scholar 

  14. Vieau D. Perinatal nutritional programming of health and metabolic adult disease. World J Diabetes 2011;2:133–136.

    Article  PubMed  Google Scholar 

  15. Vickers MH. Developmental programming of the metabolic syndrome — critical windows for intervention. World J Diabetes 2011;2:137–148.

    Article  PubMed  Google Scholar 

  16. Pinney SE, Jaeckle Santos LJ, Han Y, Stoffers DA, Simmons RA. Exendin-4 increases histone acetylase activity and reverses epigenetic modifications that silence Pdx1 in the intrauterine growth retarded rat. Diabetologia 2011;54:2606–2614.

    Article  PubMed  CAS  Google Scholar 

  17. Holness MJ, Caton PW, Sugden MC. Acute and long-term nutrient-led modifications of gene expression: potential role of SIRT1 as a central co-ordinator of short and longer-term programming of tissue function. Nutrition 2010;26:491–501.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Xiu-Min Wang.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Wang, XM. Early life programming and metabolic syndrome. World J Pediatr 9, 5–8 (2013). https://doi.org/10.1007/s12519-013-0403-7

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s12519-013-0403-7

Key words

Navigation