Document Detail


Vitamin A status modulates intestinal adaptation after partial small bowel resection.
MedLine Citation:
PMID:  10772187     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Intestinal adaptation after loss of functional small bowel surface area is characterized by cellular hyperplasia and increased absorptive function. Interventions to enhance the adaptive response are needed to decrease the morbidity and mortality associated with short bowel syndrome. Retinoic acid was shown to stimulate crypt cell proliferation in the adapting remnant rat ileum by 6 hours after resection. Thus, vitamin A, which is required for normal epithelial cell proliferation and differentiation and which can modulate programmed cell death, may play an important role in the adapting intestine. On the basis of these observations, the effects of vitamin A deficiency on intestinal morphology, epithelial cell proliferation, and apoptosis in the adapting intestine after resection were investigated. METHODS: Weanling male Sprague-Dawley rats fed either a vitamin A-deficient or -sufficient diet for 58 days underwent 70% proximal small bowel resection. The deficient rats were divided into cohorts that were either maintained on the experimental diet after surgery or replenished with vitamin A 20 hours before surgery and switched to the control diet after surgery. RESULTS: Ten days after resection, vitamin A-deficient rats exhibited a markedly blunted adaptive response. The adaptive increase in villus height and crypt depth was absent in the deficient rats. However, adaptive increases in crypt cell proliferation were not attenuated by vitamin A deficiency, and there were no differences in apoptotic indices. CONCLUSIONS: Vitamin A deficiency inhibits the adaptive response to partial small bowel resection, supporting a role for vitamin A in the adaptive process. Changes in cellular proliferation or programmed cell death are not sufficient to account for this inhibition. This model system will be useful for examining the role of other mechanisms, such as changes in cell-cell and cell-extracellular matrix interactions, and rates of epithelial cell migration and cell extrusion.
Authors:
D A Swartz-Basile; D C Rubin; M S Levin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  JPEN. Journal of parenteral and enteral nutrition     Volume:  24     ISSN:  0148-6071     ISO Abbreviation:  JPEN J Parenter Enteral Nutr     Publication Date:    2000 Mar-Apr
Date Detail:
Created Date:  2000-06-08     Completed Date:  2000-06-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7804134     Medline TA:  JPEN J Parenter Enteral Nutr     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  81-8     Citation Subset:  IM    
Affiliation:
Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological*
Animals
Apoptosis
Body Weight
Cell Division
Chromatography, High Pressure Liquid
Diet
Eating
Intestine, Small / drug effects,  physiology*,  surgery
Liver / drug effects,  metabolism
Male
Rats
Rats, Sprague-Dawley
Vitamin A / blood,  pharmacology*
Vitamin A Deficiency / physiopathology*
Grant Support
ID/Acronym/Agency:
DK46122/DK/NIDDK NIH HHS; DK50466/DK/NIDDK NIH HHS; T32 DK07130/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
11103-57-4/Vitamin A

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


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