Document Detail


Role of lysophosphatidylcholine in brush-border intestinal alkaline phosphatase release and restoration.
MedLine Citation:
PMID:  19407215     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intestinal alkaline phosphatase (IAP) is a brush-border membrane ectoenzyme (BBM-IAP) that is released into the lumen (L-IAP) after a high-fat diet. We examined the effects of oil feeding and the addition of mixed-lipid micelles on the formation of L-IAP in oil-fed rat intestine, Caco-2 cell monolayers, and mouse intestinal loops. We localized IAP in the duodenum of rats fed corn oil using fluorescence microscopy with enzyme-labeled fluorescence-97 as substrate. Four hours after oil feeding, L-IAP increased approximately 10-fold accompanied by the loss of BBM-IAP, consistent with BBM-IAP release. Rat IAP isozyme mRNAs progressively increased 4-6 h after oil feeding, followed by the increase of IAP activity in the subapical location at 6 h, consistent with the restoration of IAP protein. Postprandial lipid-micelle components, sodium taurocholate with or without oleic acid, mono-oleylglycerol, cholesterol, or lysophosphatidylcholine (lysoPC) were applied singly or as mixed-lipid micelles to the apical surface of polarized Caco-2 cell monolayers. LysoPC increased L-IAP >10-fold over basal release. LysoPC released IAP into the apical medium more than other intestinal brush-border enzymes, 5'-nucleotidase, sucrase, aminopeptidase N, and lactase, without comparable lactate dehydrogenase release or cell injury. LysoPC increased human IAP mRNA levels by 1.5-fold in Caco-2 cells. Luminally applied lysoPC also increased release of IAP preferentially in mouse intestinal loops. These data show that lysoPC accelerates the formation of L-IAP from BBM-IAP, followed by enhanced IAP synthesis, suggesting the role that lysoPC might play in the turnover of brush-border proteins.
Authors:
Takanari Nakano; Ikuo Inoue; David H Alpers; Yasutada Akiba; Shigehiro Katayama; Rina Shinozaki; Jonathan D Kaunitz; Susumu Ohshima; Masumi Akita; Seiichiro Takahashi; Iwao Koyama; Makoto Matsushita; Tsugikazu Komoda
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-04-30
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  297     ISSN:  1522-1547     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-29     Completed Date:  2009-08-04     Revised Date:  2011-02-21    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G207-14     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, Biomedical Research Center, Saitama Medical University, Saitama, Japan. nk.takanari@gmail.com
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MeSH Terms
Descriptor/Qualifier:
Alkaline Phosphatase / genetics,  metabolism*
Animals
Antigens, Neoplasm / metabolism
Caco-2 Cells
Corn Oil / administration & dosage*
Duodenum / enzymology
Epithelial Cells / enzymology
GPI-Linked Proteins
Humans
Intestines / enzymology*
Isoenzymes
Lysophosphatidylcholines / metabolism*
Male
Mice
Mice, Inbred C57BL
Micelles
Microvilli / enzymology
Postprandial Period
Protein Transport
RNA, Messenger / metabolism
Rats
Rats, Wistar
Time Factors
Grant Support
ID/Acronym/Agency:
DK56341/DK/NIDDK NIH HHS; P30 DK056341-08/DK/NIDDK NIH HHS; R01 DK54221/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, Neoplasm; 0/GPI-Linked Proteins; 0/Isoenzymes; 0/Lysophosphatidylcholines; 0/Micelles; 0/RNA, Messenger; 8001-30-7/Corn Oil; EC 3.1.3.1/ALPI protein, human; EC 3.1.3.1/Alkaline Phosphatase

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


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