Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Neither GLUT4 mRNA nor protein concentration correlated with the degree of glycemic control, fasting plasma insulin or glucose, diabetes duration, body mass index, sex, or age.
|
2354749 |
1990 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Suppression of GLUT 4 mRNA is observed in patients with impaired glucose tolerance, and therefore, may occur early in the evolution of diabetes.
|
1999488 |
1991 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
There was no significant correlation between GLUT4 polypeptide levels and HbA1c, fasting plasma glucose, insulin, or free fatty acids, daily insulin dose, duration of diabetes, or subject age but in IDDM subjects GLUT4 protein levels correlated negatively with body mass index.
|
1569156 |
1992 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In these animals, STZ-induced diabetes resulted in a parallel decrease in endogenous mouse GLUT4 mRNA and the transgenic human GLUT4 mRNA in white adipose tissue, brown adipose tissue, and cardiac muscle.
|
8486663 |
1993 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
48 h fasting decreased GLUT-4 mRNA to 23% of control with restoration beginning by 6 h refeeding and full restoration at 24 h. In contrast, ob mRNA decreased less markedly to 47% of control with only partial restoration by 24 h. Two days of streptozocin (STZ)-diabetes (glucose > 400 mg/100 ml) decreased GLUT-4 mRNA to 8% of control with restoration by two days of S.C. insulin.
|
8607798 |
1996 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
GLUT4 expression is up-regulated by exercise training and thyroid hormone treatment and is down-regulated by fasting, streptozotocin-induced diabetes, obesity, high-fat diet, and denervation.
|
9405224 |
1997 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Myocyte enhancer factor 2 (MEF2)-binding site is required for GLUT4 gene expression in transgenic mice. Regulation of MEF2 DNA binding activity in insulin-deficient diabetes.
|
9603935 |
1998 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
The increase in muscle GLUT4 in trained individuals contributes to an increase in the responsiveness of muscle glucose uptake to insulin, although not all studies show that exercise training in patients with diabetes improves overall glucose control.
|
9509261 |
1998 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
The hypothesis that altered metabolism plays a causative role in diabetes-induced contractile dysfunction was tested using perfused hearts from transgenic db/db mice that overexpress GLUT-4 glucose transporters.
|
11052966 |
2000 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
GLUT4 overexpression in db/db mice dose-dependently ameliorates diabetes but is not a lifelong cure.
|
11246879 |
2001 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We found the most sensitive and reliable molecular indicator of dioxin-induced diabetes to be the ratio of mRNA of glucose transporter 4 (GLUT4) and nuclear transcription factor kappa B (NFkappaB), a marker of inflammation.
|
17107852 |
2006 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings implicate the muscular GLUT4 system in the glucose intolerance of liver cirrhosis by a mechanism different from that in diabetes.
|
17448565 |
2007 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Downregulation of human and mouse adipose tissue GLUT4 occurs early in diabetes development.
|
22466288 |
2012 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Total GLUT4 content of the heart was decreased during diabetes, while there was no difference in total GLUT12.
|
23041416 |
2013 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Yet, the role of adipose tissue GLUT4 deregulation in the pathogenesis of insulin resistance, obesity, and diabetes is still unclear.
|
21604201 |
2013 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Insulin-mediated translocation of GLUT4 involves the PI3K/Akt kinase signal cascade that results in activation of endothelial NO synthase (eNOS). eNOS is dysfunctional during diabetes.
|
24157451 |
2014 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Defects in translocation of the glucose transporter GLUT4 are associated with peripheral insulin resistance, preclinical diabetes, and progression to type 2 diabetes.
|
28972183 |
2017 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
We suggest that sortilin- and retromer-mediated Glut4 retrieval from endosomes may represent a step in the Glut4 pathway vulnerable to the development of insulin resistance and diabetes.
|
28450454 |
2017 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Understanding the interaction between insulin signaling molecules and key regulatory proteins that are involved in spatiotemporal regulation of GLUT4 vesicle exocytosis is of great importance to explain the pathogenesis of diabetes and may provide new potential therapeutic targets.
|
28529958 |
2017 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Also, GLUT4, insulin receptor (IRβ), acetyl coenzyme A (ACC), etc. increased in fat pad of maternal offspring of diabetes.
|
28925477 |
2017 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
The inability of cells to mobilize the specific glucose transporter GLUT4 is believed to be at least partially accountable for diseases, like diabetes, where cells do not respond to an insulin stimulus.
|
28853753 |
2017 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The compounds were tested in vitro against a set of four protein targets identified as key elements in diabetes: G protein-coupled receptor 40 (GPR40), aldose reductase (AKR1B1), peroxisome proliferator-activated receptor gama (PPARγ) and solute carrier family 2 (facilitated glucose transporter), member 4 (GLUT-4).
|
29415496 |
2018 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
The mAbs identified here will be valuable molecular tools for monitoring GLUT4 structure, function, and trafficking, for differentiating GLUT4 conformational states, and for the development of novel therapeutics for the treatment of diabetes.
|
29769329 |
2018 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These findings reveal the role of gallic acid in E. officinalis mediated antidiabetic potential, and delineate the upregulation of pAkt, PPAR-γ and Glut4 in gallic acid mediated antidiabetic activity, thus providing potential therapy for diabetes and related disorders.
|
31064680 |
2019 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study reveals that increased H3K9me3 in the Slc2a4 promoter enhancer segment contributes to reduce GLUT4 expression in skeletal muscle and to worse glycemic control in diabetes, pointing to the H3K9me3 of Slc2a4 promoter as a potential target for development of new approaches for treating diabetes.
|
30528377 |
2019 |