Document Detail

Dexamethasone selectively increases sodium-dependent alanine transport across neonatal piglet intestine.
MedLine Citation:
PMID:  3502267     Owner:  NLM     Status:  MEDLINE    
1. Lysine and alanine uptake by pig enterocytes has been measured in piglet mid intestine both during normal development and 3 days after injection of dexamethasone and epidermal growth factor (EGF) into 3-day-old animals. 2. Alanine uptake measured in the presence of sodium increased markedly during the first 4 weeks of post-natal life. Similar effects on alanine uptake could be produced through injection of dexamethasone, but not EGF, into 3-day-old piglets. Alanine uptake measured in the absence of sodium and lysine uptake measured in the presence of sodium remained unchanged during development and unaffected by injection of dexamethasone or EGF. 3. Enterocytes capable of transporting alanine in the presence of sodium were found, by quantitative autoradiography, to cover the top 400 micron of the villus in 6-day-old and 3-4-week-old control pigs. Alanine concentrations in villus tip enterocytes in 3-4-week-old pigs were four times those found in 6-day-old animals. Qualitative examination of selected villi, however, showed alanine uptake taking place over a considerably greater area of villus surface in 6-day-old compared with 3-4-week-old animals. 4. Injection of dexamethasone and EGF into 3-day-old piglets caused an increase in crypt depth without apparent change in crypt cell proliferation. The rate at which enterocytes migrated out of the crypt and the length of individual villi also remained unchanged by dexamethasone or EGF injection. 5. Dexamethasone produces its effect on alanine uptake by acting on older enterocytes present on the upper part of the villus. These enterocytes can be shown, by calculations based on enterocyte migration rate, to have already been present on the villus at the time the pig was born. 6. The above findings are discussed in relation to the ability of villus as well as crypt enterocytes to change their programme of differentiation in response to external stimuli. The particular ability of dexamethasone to induce system A type carrier function is further discussed in relation to normal changes found to occur during neonatal development. It is finally suggested, as a working hypothesis, that endogenous glucagon might act as the final mediator of both developmentally controlled and dexamethasone-induced changes in amino acid transport.
P S James; M W Smith; D R Tivey; T J Wilson
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of physiology     Volume:  393     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  1987 Dec 
Date Detail:
Created Date:  1988-05-13     Completed Date:  1988-05-13     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  569-82     Citation Subset:  IM    
Agricultural and Food Research Council, Institute of Animal Physiology and Genetics Research, Babraham, Cambridge.
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MeSH Terms
Alanine / pharmacokinetics*
Animals, Newborn / metabolism*
Biological Transport / drug effects
Cell Division / drug effects
Dexamethasone / pharmacology*
Epidermal Growth Factor / pharmacology
Intestinal Mucosa / drug effects,  metabolism
Intestine, Small / drug effects,  metabolism*
Sodium / pharmacology*
Swine / metabolism*
Reg. No./Substance:
50-02-2/Dexamethasone; 56-41-7/Alanine; 62229-50-9/Epidermal Growth Factor; 7440-23-5/Sodium

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

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