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This review will summarize the effects of phytochemicals and their action on insulin (Montrer INS Protéines) signaling pathways accelerating GLUT4 translocation based on the current literature.
Our results demonstrate that IR is associated with high circulating RBP4 (Montrer POLR2D Protéines) and that suppressed RBP4 (Montrer POLR2D Protéines) adipose tissue expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF (Montrer Vcan Protéines) are effective in lowering serum RBP4 (Montrer POLR2D Protéines) levels.
Cell-autonomous adiposity results from increased cell surface GLUT4 due to ankyrin-B deficiency in humans and mice.
The authors show that insulin (Montrer INS Protéines)-stimulated Glut4-mediated glucose uptake requires PDPK1 (Montrer PDPK1 Protéines) phosphorylation of the kinase domain but not mTORC2 (Montrer CRTC2 Protéines) phosphorylation of the hydrophobic domain. Nonetheless, an intact hydrophobic domain is required for Glut4-mediated glucose uptake.
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 (Montrer SCD Protéines), SLC2A4, and SREBF1 (Montrer SREBF1 Protéines) 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 (Montrer SLC2A1 Protéines), GLUT-4 and GLUT-9 proteins in the trophoblast from both, uncomplicated and diabetic pregnancies. In addition, insulin (Montrer INS Protéines) therapy may increase placental expression of GLUT-4 and GLUT-9, and partially GLUT-1 (Montrer SLC2A1 Protéines), 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 (Montrer INS Protéines) additive analogue.
studies demonstrate that Elmo2 (Montrer ELMO2 Protéines) is a new regulator of insulin (Montrer INS Protéines)-dependent Glut4 membrane translocation through modulating Rac1 activity and Akt (Montrer AKT1 Protéines) membrane compartmentalization.
Feed intake remains low whereas respiratory frequency and body temperature remain higher and expression of HSP90 (Montrer HSP90 Protéines), CAT1 (Montrer SLC7A1 Protéines), SGLT1 (Montrer SLC5A1 Protéines) and GLUT4 increases in some tissues in pigs under chronic heat stress conditions.
TBC1D4 (Montrer TBC1D4 Protéines), insulin receptor (Montrer INSR Protéines) and GLUT4 showed altered expression in some tissues in pre-diabetic pigs.
analysis of time- and breed-specific expression patterns of GLUT2 (Montrer SLC2A2 Protéines) and GLUT4, which highlight their potential as candidate genes for assessing adipose deposition and muscle development in pigs
Chronic elevated calcium blocks AMPK (Montrer PRKAA1 Protéines)-induced GLUT-4 expression in skeletal muscle.
Insulin (Montrer INS Protéines) 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.
1,2-dioleoyl-sn-glycero-3-phosphoethanolamine retains cell surface GLUT4 by suppressing PKC alpha (Montrer PKCa Protéines)-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 (Montrer SIRT1 Protéines) activation, which in turn increases IRS1 (Montrer IRS1 Protéines) phosphorylation and GLUT4 translocation in myotubes.
G4+/- offspring on a High Fat Diet displayed early hypertension associated with increased renal gene expression of renin (Montrer REN Protéines) and the AT1 (Montrer SLC33A1 Protéines)- 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 (Montrer DNM1 Protéines) is a molecular motor (Montrer MYO1B Protéines) which would be involved in GLUT4 translocation by facilitating exocytosis
Insulin (Montrer INS Protéines)-stimulated translocation of GLUT4 and GLUT8 (Montrer SLC2A8 Protéines) was down-regulated in the atria of insulin (Montrer INS Protéines) 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 (Montrer FDXR Protéines) levels; high glucose availability up-regulates total NADH/NADPH (Montrer FDXR Protéines) 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 (Montrer TBK1 Protéines) directly interacts with Exo84 (Montrer EXO84 Protéines) through the coiled-coil domain of TBK1 (Montrer TBK1 Protéines) and helical domain of Exo84 (Montrer EXO84 Protéines), and knockdown of TBK1 (Montrer TBK1 Protéines) blocked insulin (Montrer INS Protéines)-stimulated glucose uptake and GLUT4 translocation.
Low GLUT1 (Montrer SLC2A1 Protéines) and GLUT3 (Montrer SLC2A3 Protéines) expression in nonclassical monocytes was unaltered during differentiation into macrophages. GLUT4 mRNA was only detectable in unstimulated macrophages. Neither monocytes nor macrophages were insulin (Montrer INS Protéines) responsive.
Results of the present study suggest that myostatin (Montrer MSTN Protéines) 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 (Montrer INS Protéines) 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