Document Detail


Accelerated senescence in kidneys of low-birth-weight rats after catch-up growth.
MedLine Citation:
PMID:  19828676     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epidemiological studies show a strong association between low birth weight and hypertension, renal, and cardiovascular disease, especially after catch-up growth. Senescence is an important contributor to the progression of chronic disease. Developmentally programmed premature senescence may be a link among low birth weight, catch-up growth, and adult disease. Low birth weight was induced by feeding pregnant rats a low-protein diet from day 12 of gestation to 10 days postdelivery. Low- and normal-birth-weight male offspring were weaned onto regular or high-calorie diets to enhance catch-up growth. Kidneys and hearts of offspring were analyzed for RNA and protein markers of stress-induced senescence (p16, p21, p53, Rb). Markers of mitochondrial stress (p66Shc) and activation of endoplasmic reticulum protein secretion (Ero1alpha) were analyzed as regulators of reactive oxygen species generation. Reactive oxygen species are known to be associated with premature aging. Senescence markers were not different in low- or normal-birth-weight kidneys at birth. During rapid catch-up growth, p16 and p21 increased significantly in low-birth-weight kidneys and hearts (P < 0.01). Renal p16 levels increased progressively and were significantly higher in low-birth-weight kidneys at 3 and 6 mo (P < or = 0.02). Renal p66Shc and Ero1alpha were significantly higher in low- compared with normal- birth-weight kidneys at 6 mo, suggesting reactive oxygen species generation (P < or = 0.03). Low-birth-weight rats exhibit accelerated senescence in kidneys and hearts after rapid catch-up growth, a likely important link between early growth and subsequent hypertension, renal, and cardiovascular disease.
Authors:
Valerie A Luyckx; Catharine A Compston; Thomas Simmen; Thomas F Mueller
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-10-14
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  297     ISSN:  1522-1466     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-25     Completed Date:  2009-12-28     Revised Date:  2011-04-28    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F1697-705     Citation Subset:  IM    
Affiliation:
Division of Nephrology, University of Alberta, Edmonton, Alberta, Canada. vluyckx@ualberta.ca
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MeSH Terms
Descriptor/Qualifier:
Aging / metabolism
Aging, Premature / complications*
Animals
Animals, Newborn / growth & development*
Biological Markers / metabolism
Birth Weight*
Cardiovascular Diseases / etiology*
Cyclin-Dependent Kinase Inhibitor p16 / metabolism
Diet
Energy Intake
Female
Gene Expression
Kidney / growth & development*,  metabolism
Kidney Diseases / etiology*
Male
Myocardium / metabolism
Oxidoreductases / metabolism
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species / metabolism
Retinoblastoma Protein / metabolism
Shc Signaling Adaptor Proteins / metabolism
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Cyclin-Dependent Kinase Inhibitor p16; 0/Reactive Oxygen Species; 0/Retinoblastoma Protein; 0/Shc Signaling Adaptor Proteins; 0/Shc1 protein, rat; EC 1.-/Oxidoreductases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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