Use of GLUT-4 null mice to study skeletal muscle glucose uptake

被引:14
作者
Charron, MJ
Gorovits, N
Laidlaw, JS
Ranalletta, M
Katz, EB
机构
[1] Yeshiva Univ Albert Einstein Coll Med, Dept Biochem, Bronx, NY 10461 USA
[2] Yeshiva Univ Albert Einstein Coll Med, Dept Obstet & Gynecol & Womens Hlth, Bronx, NY 10461 USA
关键词
glucose transporter; glucose uptake; GLUT-4; insulin action; skeletal muscle;
D O I
10.1111/j.1440-1681.2005.04189.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
1. The present review focuses on the effects of varying levels of GLUT-4, the insulin-senstive glucose transporter, on insulin sensitivity and whole body glucose homeostasis. 2. Three mouse models are discussed including myosin light chain (MLC)-GLUT-4 mice which overexpress GLUT-4 specifically in skeletal muscle, GLUT-4 null mice which express no GLUT-4 and the MLC-GLUT-4 null mice which express GLUT-4 only in skeletal muscle. Overexpressing GLUT-4 specifically in the skleletal muscle results in increased insulin sensitivity in the MLC-GLUT-4 mice. In contrast, the GLUT-4 null mice exhibit insulin intolerance accompanied by abnormalities in glucose and lipid metabolism. Restoring GLUT-4 expression in skeletal muscle in the MLC-GLUT-4 null mice results in normal glucose metabolism but continued abnormal lipid metabolism. 3. The results of experiments using these mouse models demonstrates that modifying the expresssion of GLUT-4 profoundly affects whole body insulin action and consequently glucose and lipid metabolism.
引用
收藏
页码:308 / 313
页数:6
相关论文
共 45 条
[1]   Adipose-selective targeting of the GLUT4 gene impairs insulin action in muscle and liver [J].
Abel, ED ;
Peroni, O ;
Kim, JK ;
Kim, YB ;
Boss, O ;
Hadro, E ;
Minnemann, T ;
Shulman, GI ;
Kahn, BB .
NATURE, 2001, 409 (6821) :729-733
[2]   Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart [J].
Abel, ED ;
Kaulbach, HC ;
Tian, R ;
Hopkins, JCA ;
Duffy, J ;
Doetschman, T ;
Minnemann, T ;
Boers, ME ;
Hadro, E ;
Oberste-Berghaus, C ;
Quist, W ;
Lowell, BB ;
Ingwall, JS ;
Kahn, BB .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (12) :1703-1714
[3]   FORCE-VELOCITY RELATIONS AND MYOSIN HEAVY-CHAIN ISOFORM COMPOSITIONS OF SKINNED FIBERS FROM RAT SKELETAL-MUSCLE [J].
BOTTINELLI, R ;
SCHIAFFINO, S ;
REGGIANI, C .
JOURNAL OF PHYSIOLOGY-LONDON, 1991, 437 :655-672
[4]   GLUT4 gene regulation and manipulation [J].
Charron, MJ ;
Katz, EB ;
Olson, AL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (06) :3253-3256
[5]   Signaling mechanisms that regulate glucose transport [J].
Czech, MP ;
Corvera, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (04) :1865-1868
[6]   THE EFFECT OF INSULIN ON THE DISPOSAL OF INTRAVENOUS GLUCOSE - RESULTS FROM INDIRECT CALORIMETRY AND HEPATIC AND FEMORAL VENOUS CATHETERIZATION [J].
DEFRONZO, RA ;
JACOT, E ;
JEQUIER, E ;
MAEDER, E ;
WAHREN, J ;
FELBER, JP .
DIABETES, 1981, 30 (12) :1000-1007
[7]   THE TRIUMVIRATE - BETA-CELL, MUSCLE, LIVER - A COLLUSION RESPONSIBLE FOR NIDDM [J].
DEFRONZO, RA .
DIABETES, 1988, 37 (06) :667-687
[8]   Muscle glycogen content affects insulin-stimulated glucose transport and protein kinase B activity [J].
Derave, W ;
Hansen, BF ;
Lund, S ;
Kristiansen, S ;
Richter, EA .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2000, 279 (05) :E947-E955
[9]  
Galuska D, 1998, ADV EXP MED BIOL, V441, P73
[10]   Exercise, glucose transport, and insulin sensitivity [J].
Goodyear, LJ ;
Kahn, BB .
ANNUAL REVIEW OF MEDICINE, 1998, 49 :235-261