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Autophagy and GLUT4 utilise similar proteins (SNAREs) which are used for exocytosis. PI3K and AMPK control both autophagy and GLUT4. [review]
Higher expression of GLUT-4 is associated with Oral Epithelial Dysplasia compared to Oral Squamous Cell Carcinoma.
Adipose tissue sirtuin 1 was related to insulin sensitivity. The relationship was still present after controlling for BMI, however, it disappeared after controlling for adipose tissue SLC2A4. Muscle sirtuin 1 was not related to insulin sensitivity.
Results showed that GLUT4 translocation is regulated by TBC1D15 affecting glucose uptake.
This review will summarize the effects of phytochemicals and their action on insulin signaling pathways accelerating GLUT4 translocation based on the current literature.
Our results demonstrate that IR is associated with high circulating RBP4 and that suppressed RBP4 adipose tissue expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF are effective in lowering serum RBP4 levels.
Cell-autonomous adiposity results from increased cell surface GLUT4 due to ankyrin-B deficiency in humans and mice.
The authors show that insulin-stimulated Glut4-mediated glucose uptake requires PDPK1 phosphorylation of the kinase domain but not mTORC2 phosphorylation of the hydrophobic domain. Nonetheless, an intact hydrophobic domain is required for Glut4-mediated glucose uptake.
rs5435 was not associated with T1D in the Euro-Brazilian population.
Three polymorphisms (rs2654185, rs5415, and rs5417) in SLC2A4 were positively correlated with hip circumference and the rs2654185 locus was also positively associated with thigh circumference. Consumption of n-3 polyunsaturated fatty acids modifies associations between SCD, SLC2A4, and SREBF1 polymorphisms and anthropometric variables and metabolic phenotypes.
increased GLUT4 expression in oral squamous cell carcinoma patients was significantly associated with a poor overall survival (OS, P = 0.035) and recurrence-free survival (RFS, P = 0.001). Furthermore, the ectopic overexpression of GLUT4 in cell lines with low endogenous GLUT4 expression resulted in a significant increase in migratory ability both in vitro and in vivo
The results of the study confirmed the presence of GLUT-1, GLUT-4 and GLUT-9 proteins in the trophoblast from both, uncomplicated and diabetic pregnancies. In addition, insulin therapy may increase placental expression of GLUT-4 and GLUT-9, and partially GLUT-1, in women with pregestational and gestational diabetes mellitus.
our study has found that BMI, hypertension, myometrial invasion, pathological type, and Glut4 positive expression might be prognostic factors of EC [Endometrial cancer ]
Our work highlights the convenience and efficiency of this novel pH-sensitive fluorescent probe and reveals the new biological activity of staurosporine as an agonist for GLUT4 translocation and as an effective insulin additive analogue.
studies demonstrate that Elmo2 is a new regulator of insulin-dependent Glut4 membrane translocation through modulating Rac1 activity and Akt membrane compartmentalization.
This review focuses on recent advances on the role of these signaling pathways and transcription factors involved in the regulation of CD36 and GLUT4.
effects of physiologically relevant phospholipids on glucose transport in liposomes containing purified GLUT4 and GLUT3. The anionic phospholipids, phosphatidic acid, phosphatidylserine, phosphatidylglycerol, and phosphatidylinositol, were found to be essential for transporter function by activating it and stabilizing its structure.
These results suggest that the initial event caused by overnutrition may be oxidative stress, which produces insulin resistance, at least in part, via carbonylation and oxidation-induced inactivation of GLUT4.
A single bout of exercise elicited similar GLUT4 translocation in skeletal muscle of PCOS and Controls. The absence of impairment in GLUT4 translocation suggests that PCOS patients with obesity and insulin resistance may benefit from exercise training.
SLC2A4 gene expression level was slightly lower within type 2 diabetic patients in both type of tissues. Furthermore, the negative correlation between SLC2A4 gene expression level in visceral adipose tissue and BMI has been noticed
Feed intake remains low whereas respiratory frequency and body temperature remain higher and expression of HSP90, CAT1, SGLT1 and GLUT4 increases in some tissues in pigs under chronic heat stress conditions.
TBC1D4, insulin receptor and GLUT4 showed altered expression in some tissues in pre-diabetic pigs.
analysis of time- and breed-specific expression patterns of GLUT2 and GLUT4, which highlight their potential as candidate genes for assessing adipose deposition and muscle development in pigs
Chronic elevated calcium blocks AMPK-induced GLUT-4 expression in skeletal muscle.
Insulin resistance was associated with a significantly reduced total GLUT4 content in omental adipose tissue, without a change in content in other visceral or subcutaneous adipose sites.
There was a significant difference when pooled means for Glut-4 expression in muscle compared with adipose tissue from different anatomical sites.
beta-catenin is a previously unrecognized regulator of the mechanisms that control the insulin sensitive pool of GLUT4 transporters inside these adipocyte cells.
The study shows a novel role of leptin-induced P2X7r in modulating Glut4 induction and translocation in hepatic stellate cells, that are key to nonalcoholic steatohepatitis progression.
ESR1 activation in adipocytes increased the nuclear content of SP1 protein, the SP1/ESR1 interaction and SP1 binding into the Slc2a4 gene promoter, culminating with increased Slc2a4/GLUT4 expression
Those findings provide new insight into the mechanisms responsible for AMPKalpha2-dependent regulation of GLUT4 transcription after exercise.
Portulaca oleracea L. extract enhanced glucose uptake, which was caused by increased GLUT4 expression at the plasma membrane through activating the PI3K/Akt pathway.
1,2-dioleoyl-sn-glycero-3-phosphoethanolamine retains cell surface GLUT4 by suppressing PKC alpha-driven endocytic internalization of GLUT4, to enhance glucose uptake into cells and restrict an increase in the blood glucose levels after glucose loading in type 2 Diabetes Mellitus.
The data, therefore, suggest that 1,25(OH)2D3 increases glucose consumption by inducing SIRT1 activation, which in turn increases IRS1 phosphorylation and GLUT4 translocation in myotubes.
G4+/- offspring on a High Fat Diet displayed early hypertension associated with increased renal gene expression of renin and the AT1- receptors compared to G4+/- on a C diet. This group showed decreased cardiac expression of key genes involved in fatty acid oxidation compared to WT on a C diet.
dynamin is a molecular motor which would be involved in GLUT4 translocation by facilitating exocytosis
Insulin-stimulated translocation of GLUT4 and GLUT8 was down-regulated in the atria of insulin resistance animals, as well as their total protein expression.
The disruption of SM22alpha enhances PDGF-BB-induced GLUT4 translocation and glucose uptake by promoting actin dynamics and cortical actin polymeriza- tion.
Data suggest that Glut4 expression is glucose-dependent in white adipocytes; low glucose availability reduces total NADH/NADPH levels; high glucose availability up-regulates total NADH/NADPH levels, promotes adipogenesis and lipogenesis, and induces Glut4 expression.
Glucose transporter 4 (GLUT4) is required for myocardial adaptations to exercise, and its absence accelerates heart dysfunction after pressure overload.
Data show that TBK1 directly interacts with Exo84 through the coiled-coil domain of TBK1 and helical domain of Exo84, and knockdown of TBK1 blocked insulin-stimulated glucose uptake and GLUT4 translocation.
E4-ORF1 activation of PI3K in adipocytes recapitulates insulin regulation of FoxO1 but not regulation of Glut4. This uncoupling of PI3K effects occurs despite E4-ORF1 activating PI3K and downstream signaling to levels achieved by insulin.
Authors 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.
It was concluded that ILK depletion modifies the transcription of GLUT4, which results in reduced peripheral insulin sensitivity and glucose uptake, suggesting ILK as a molecular target and a prognostic biomarker of insulin resistance.
Data, including data from studies using knockout/transgenic mice, suggest that PrPC is involved in development of insulin resistance and obesity; primary embryonic fibroblasts cultured from PrPC knockout mice exhibit reduced glucose uptake upon insulin stimulation due to reduced translocation of glucose transporter Glut4 to cell membrane. (PrPC = cellular prion protein; Glut4 = facilitated glucose transporter 4)
Our findings implicate Rac1 as a regulatory element critical for controlling glucose uptake during exercise via regulation of GLUT4 translocation.
Low GLUT1 and GLUT3 expression in nonclassical monocytes was unaltered during differentiation into macrophages. GLUT4 mRNA was only detectable in unstimulated macrophages. Neither monocytes nor macrophages were insulin responsive.
Results of the present study suggest that myostatin inhibits the expression of GLUT4 mRNA and that the greater ability of double muscled cattle to produce muscle may be due to their greater sensitivity to insulin and greater use of glucose.
GLUT4 gene expression increased during late lactation.
These results suggest that goat GLUT4 functions in the transport of glucose and it may play a positive role in amino acid uptake in mammary glands.
This gene is a member of the solute carrier family 2 (facilitated glucose transporter) family and encodes a protein that functions as an insulin-regulated facilitative glucose transporter. In the absence of insulin, this integral membrane protein is sequestered within the cells of muscle and adipose tissue. Within minutes of insulin stimulation, the protein moves to the cell surface and begins to transport glucose across the cell membrane. Mutations in this gene have been associated with noninsulin-dependent diabetes mellitus (NIDDM).
, glucose transporter type 4, insulin-responsive
, insulin-responsive glucose transporter type 4
, solute carrier family 2, facilitated glucose transporter member 4
, glucose transporter 4
, glucose transporter type 4
, solute carrier family 2 (facilitated glucose transporter), member 4
, solute carrier family 2, facilitated glucose transporter member 4-like
, Insulin-responsive glucose transporter
, insulin-responsive glucose transporter 4
, insulin-responsive glucose transporter
, Glucose transporter 4 insuline-responsive
, Glucose transporter 4, insuline-responsive
, solute carrier family 2 member 4
, solute carrier family 2 , member 4