Munc18c provides stimulus-selective regulation of GLUT4 but not fatty acid transporter trafficking in skeletal muscle

被引:13
|
作者
Jain, Swati S. [1 ]
Snook, Laelie A. [1 ]
Glatz, Jan F. C. [2 ]
Luiken, Joost J. F. P. [2 ]
Holloway, Graham P. [1 ]
Thurmond, Debbie C. [3 ]
Bonen, Arend [1 ]
机构
[1] Univ Guelph, Dept Human Hlth & Nutr Sci, Guelph, ON N1G 2W1, Canada
[2] Maastricht Univ, Dept Mol Genet, Cardiovasc Res Inst Maastricht CARIM, NL-6200 MD Maastricht, Netherlands
[3] Indiana Univ Sch Med, Herman B Wells Ctr Pediat Res, Basic Diabet Res Grp, Dept Pediat, Indianapolis, IN 46202 USA
基金
美国国家卫生研究院; 加拿大健康研究院;
关键词
FAT/CD36; FABPpm; FATP1; FATP4; Fatty acid transport; Glucose transport; OBESE ZUCKER RAT; GLUCOSE-UPTAKE; TRANSLOCASE (FAT)/CD36; PALMITATE OXIDATION; 3T3-L1; ADIPOCYTES; INSULIN; MEMBRANE; FAT/CD36; IDENTIFICATION; VESICLES;
D O I
10.1016/j.febslet.2012.05.061
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Insulin-, and contraction-induced GLUT4 and fatty acid (FA) transporter translocation may share common trafficking mechanisms. Our objective was to examine the effects of partial Munc18c ablation on muscle glucose and FA transport, FA oxidation, GLUT4 and FA transporter (FAT/CD36, FAB-Ppm, FATP1, FATP4) trafficking to the sarcolemma, and FAT/CD36 to mitochondria. In Munc18c(-/+) mice, insulin-stimulated glucose transport and GLUT4 sarcolemmal appearance were impaired, but were unaffected by contraction. Insulin- and contraction-stimulated FA transport, sarcolemmal FA transporter appearance, and contraction-mediated mitochondrial FAT/CD36 were increased normally in Munc18c(-/+) mice. Hence, Munc18c provides stimulus-specific regulation of GLUT4 trafficking, but not FA transporter trafficking. (c) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:2428 / 2435
页数:8
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