GLUT4Gene Regulation and Manipulation

Charron, Maureen J.; Katz, Ellen B.; Olson, Ann Louise

doi:10.1074/jbc.274.6.3253

Cited by 128 publications

(92 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As reviewed recently (1,2), there are many hormones or stimuli reported to regulate glucose transport. Insulin stimulation of glucose transport has received considerable study and the signaling pathways involved are understood in more detail than other regulators of glucose transport.…”

Section: Discussionmentioning

confidence: 99%

Preconditioning Enhanced Glucose Uptake Is Mediated by p38 MAP Kinase Not by Phosphatidylinositol 3-Kinase

Tong¹,

Chen²,

London

et al. 2000

Journal of Biological Chemistry

View full text Add to dashboard Cite

Ischemia is reported to stimulate glucose uptake, but the signaling pathways involved are poorly understood. Modulation of glucose transport could be important for the cardioprotective effects of brief intermittent periods of ischemia and reperfusion, termed ischemic preconditioning. Previous work indicates that preconditioning reduces production of acid and lactate during subsequent sustained ischemia, consistent with decreased glucose utilization. However, there are also data that preconditioning enhances glucose uptake. The present study examines whether preconditioning alters glucose transport and whether this is mediated by either phosphatidylinositol 3-kinase (PI3K) or p38 MAP kinase. Langendorff-perfused rat hearts were preconditioned with 4 cycles of 5 min of ischemia and 5 min of reperfusion, with glucose as substrate. During the last reflow, glucose was replaced with 5 mM acetate and 5 mM 2-deoxyglucose (2DG), and hexose transport was measured from the rate of production of 2-deoxyglucose 6-phosphate (2DG6P), using 31 P nuclear magnetic resonance. Preconditioning stimulated 2DG uptake; after 15 min of perfusion with 2DG, 2DG6P levels were 165% of initial ATP in preconditioned hearts compared with 96% in control hearts (p < 0.05). Wortmannin, an inhibitor of PI3K, did not block the preconditioning induced stimulation of 2DG6P production, but perfusion with SB202190, an inhibitor of p38 MAP kinase, did attenuate 2DG6P accumulation (111% of initial ATP, p < 0.05 compared with preconditioned hearts). SB202190 had no effect on 2DG6P accumulation in nonpreconditioned hearts. Preconditioning stimulation of translocation of GLUT4 to the plasma membrane was not inhibited by wortmannin. The data demonstrate that ischemic preconditioning increases hexose transport and that this is mediated by p38 MAP kinase and is PI3K-independent.

show abstract

Section: Discussionmentioning

confidence: 99%

Preconditioning Enhanced Glucose Uptake Is Mediated by p38 MAP Kinase Not by Phosphatidylinositol 3-Kinase

Tong¹,

Chen²,

London

et al. 2000

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Both insulin and diabetes also exert potent effects on transcription of metabolic and growth-regulatory genes in skeletal muscle, including ras-related associated with diabetes (RAD1), hexokinase 2 (HK2), and glucose transporter type 4 (GLUT4) (18)(19)(20)(21). Basal expression of these genes was significantly reduced in IR-Mut myotubes compared with controls ( Fig.…”

Section: Insulin Signaling Is Defective In Insulin-resistant Ips Cellmentioning

confidence: 99%

Myotubes derived from human-induced pluripotent stem cells mirror in vivo insulin resistance

Iovino

Burkart

Warren

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Induced pluripotent stem cells (iPS cells) represent a unique tool for the study of the pathophysiology of human disease, because these cells can be differentiated into multiple cell types in vitro and used to generate patient- and tissue-specific disease models. Given the critical role for skeletal muscle insulin resistance in whole-body glucose metabolism and type 2 diabetes, we have created a novel cellular model of human muscle insulin resistance by differentiating iPS cells from individuals with mutations in the insulin receptor (IR-Mut) into functional myotubes and characterizing their response to insulin in comparison with controls. Morphologically, IR-Mut cells differentiated normally, but had delayed expression of some muscle differentiation-related genes. Most importantly, whereas control iPS-derived myotubes exhibited in vitro responses similar to primary differentiated human myoblasts, IR-Mut myotubes demonstrated severe impairment in insulin signaling and insulin-stimulated 2-deoxyglucose uptake and glycogen synthesis. Transcriptional regulation was also perturbed in IR-Mut myotubes with reduced insulin-stimulated expression of metabolic and early growth response genes. Thus, iPS-derived myotubes from individuals with genetically determined insulin resistance demonstrate many of the defects observed in vivo in insulin-resistant skeletal muscle and provide a new model to analyze the molecular impact of muscle insulin resistance.

show abstract

“…7A, we found that the levels of GLUT-4 were dramatically increased in Cav-1 null mice, possibly as a response to the postprandial hyperinsulinemia. Other groups have previously reported that GLUT-4 levels are elevated in response to hyperinsulinemia (3,5). Furthermore, a recent report indicates that, in 3T3L1 adipocytes, disruption of caveolae with cholesterol chelating agents results in an insulin-independent increase in plasma membrane GLUT-4 (39).…”

Section: Cav-1 Null Mice Have a Primary Defect In Insulin Signaling Imentioning

confidence: 98%

Caveolin-1-deficient mice show insulin resistance and defective insulin receptor protein expression in adipose tissue

Cohen

Razani

Wang

et al. 2003

American Journal of Physiology-Cell Physiology

319

254

View full text Add to dashboard Cite

show abstract

GLUT4Gene Regulation and Manipulation

Cited by 128 publications

References 38 publications

Preconditioning Enhanced Glucose Uptake Is Mediated by p38 MAP Kinase Not by Phosphatidylinositol 3-Kinase

Preconditioning Enhanced Glucose Uptake Is Mediated by p38 MAP Kinase Not by Phosphatidylinositol 3-Kinase

Myotubes derived from human-induced pluripotent stem cells mirror in vivo insulin resistance

Caveolin-1-deficient mice show insulin resistance and defective insulin receptor protein expression in adipose tissue

Contact Info

Product

Resources

About