Document Detail

Role of fatty acid transport protein 4 in oleic acid-induced glucagon-like peptide-1 secretion from murine intestinal L cells.
MedLine Citation:
PMID:  22871340     Owner:  NLM     Status:  MEDLINE    
The antidiabetic intestinal L cell hormone glucagon-like peptide-1 (GLP-1) enhances glucose-dependent insulin secretion and inhibits gastric emptying. GLP-1 secretion is stimulated by luminal oleic acid (OA), which crosses the cell membrane by an unknown mechanism. We hypothesized that L cell fatty acid transport proteins (FATPs) are essential for OA-induced GLP-1 release. Therefore, the murine GLUTag L cell model was used for immunoblotting, [(3)H]OA uptake assay, and GLP-1 secretion assay as determined by radioimmunoassay following treatment with OA ± phloretin, sulfo-N-succinimidyl oleate, or siRNA against FATP4. FATP4(-/-) and cluster-of-differentiation 36 (CD36)(-/-) mice received intraileal OA, and plasma GLP-1 was measured by sandwich immunoassay. GLUTag cells were found to express CD36, FATP1, FATP3, and FATP4. The cells demonstrated specific (3)H[OA] uptake that was dose-dependently inhibited by 500 and 1,000 μM unlabeled OA (P < 0.001). Cell viability was not altered by treatment with OA. Phloretin and sulfo-N-succinimidyl oleate, inhibitors of protein-mediated transport and CD36, respectively, also decreased [(3)H]OA uptake, as did knockdown of FATP4 by siRNA transfection (P < 0.05-0.001). OA dose-dependently increased GLP-1 secretion at 500 and 1,000 μM (P < 0.001), whereas phloretin, sulfo-N-succinimidyl oleate, and FATP4 knockdown decreased this response (P < 0.05-0.01). FATP4(-/-) mice displayed lower plasma GLP-1 at 60 min in response to intraileal OA (P < 0.05), whereas, unexpectedly, CD36(-/-) mice displayed higher basal GLP-1 levels (P < 0.01) but a normal response to intraileal OA. Together, these findings demonstrate a key role for FATP4 in OA-induced GLP-1 secretion from the murine L cell in vitro and in vivo, whereas the precise role of CD36 remains unclear.
M A Poreba; C X Dong; S K Li; A Stahl; J H Miner; P L Brubaker
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-08-07
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  303     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-02     Completed Date:  2013-01-07     Revised Date:  2013-10-10    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E899-907     Citation Subset:  IM    
Department of Physiology, University of Toronto, Toronto, Ontario, Canada.
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MeSH Terms
Antigens, CD36 / analysis,  genetics
Cells, Cultured
Enteroendocrine Cells / drug effects,  metabolism*
Fatty Acid Transport Proteins / analysis,  blood*,  genetics
Gene Silencing
Glucagon-Like Peptide 1 / secretion*
Mice, Inbred C57BL
Oleic Acid / pharmacology*
Oleic Acids / pharmacology
Phloretin / pharmacology
Succinimides / pharmacology
Grant Support
R01 AR049269/AR/NIAMS NIH HHS; R01-AR-049269/AR/NIAMS NIH HHS; //Canadian Institutes of Health Research
Reg. No./Substance:
0/Antigens, CD36; 0/Fatty Acid Transport Proteins; 0/Oleic Acids; 0/Slc27a1 protein, mouse; 0/Slc27a4 protein, mouse; 0/Succinimides; 0/sulfo-N-succinimidyl oleate; 112-80-1/Oleic Acid; 60-82-2/Phloretin; 89750-14-1/Glucagon-Like Peptide 1

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

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