Document Detail


Update: consequences of abnormal fetal growth.
MedLine Citation:
PMID:  22238390     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intrauterine growth restriction (IUGR) is prevalent worldwide and affects children and adults in multiple ways. These include predisposition to type 2 diabetes mellitus, the metabolic syndrome, cardiovascular disease, persistent reduction in stature, and possibly changes in the pattern of puberty. A review of recent literature confirms that the metabolic effects of being born small for gestational age are evident in the very young, persist with age, and are amplified by adiposity. Furthermore, the pattern of growth in the first few years of life has a significant bearing on a person's later health, with those that show increasing weight gain being at the greatest risk for future metabolic dysfunction. Treatment with exogenous human GH is used to improve height in children who remain short after being small for gestational age at birth, but the response of individuals remains variable and difficult to predict. The mechanisms involved in the metabolic programming of IUGR children are just beginning to be explored. It appears that IUGR leads to widespread changes in DNA methylation and that specific "epigenetic signatures" for IUGR are likely to be found in various fetal tissues. The challenge is to link such alterations with modifications in gene expression and ultimately the metabolic abnormalities of adulthood, and it represents one of the frontiers for research in the field.
Authors:
Steven D Chernausek
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-01-11
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  97     ISSN:  1945-7197     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-03-06     Completed Date:  2012-07-06     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  689-95     Citation Subset:  AIM; IM    
Affiliation:
Department of Pediatrics, University of Oklahoma Health Sciences Center, 1200 North Phillips Avenue, Suite 4500, Oklahoma City, Oklahoma 73104-4600, USA. Steven-Chernausek@OUHSC.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Diabetes Mellitus, Type 2 / etiology*,  physiopathology
Fetal Growth Retardation / physiopathology*
Humans
Infant, Newborn
Infant, Small for Gestational Age
Metabolic Syndrome X / etiology*,  physiopathology
Obesity / etiology*,  physiopathology
Grant Support
ID/Acronym/Agency:
R01DK089034/DK/NIDDK NIH HHS
Comments/Corrections

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