PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33715230-4 2021 In the present study, we found that aggressive breast and prostate cancer cell lines with overactivated Akt activity exhibit enhanced glucose uptake and GLUT1 translocation upon insulin treatment, and KU-55933, a specific inhibitor of ATM, inhibits insulin-mediated glucose uptake by blocking translocation of GLUT1 to the cell surface. Glucose 266-273 thymoma viral proto-oncogene 1 Mus musculus 104-107 33999329-0 2021 Isorhamnetin Alleviates High Glucose-Aggravated Inflammatory Response and Apoptosis in Oxygen-Glucose Deprivation and Reoxygenation-Induced HT22 Hippocampal Neurons Through Akt/SIRT1/Nrf2/HO-1 Signaling Pathway. Glucose 29-36 thymoma viral proto-oncogene 1 Mus musculus 173-176 34025589-13 2021 The insulin rise caused by glucose uptake, presumably originated from the pancreas, may serve as a negative feedback to inhibit the SPX response by activating MAPK and PI3K/Akt pathways in the stomach. Glucose 27-34 thymoma viral proto-oncogene 1 Mus musculus 173-176 33906607-12 2021 CONCLUSIONS: Our results indicate that GluOC reduces the inhibitory effect of high glucose on osteoblast differentiation by regulating the TP63/PTEN/Akt/GSK3beta pathway. Glucose 83-90 thymoma viral proto-oncogene 1 Mus musculus 149-152 33715230-4 2021 In the present study, we found that aggressive breast and prostate cancer cell lines with overactivated Akt activity exhibit enhanced glucose uptake and GLUT1 translocation upon insulin treatment, and KU-55933, a specific inhibitor of ATM, inhibits insulin-mediated glucose uptake by blocking translocation of GLUT1 to the cell surface. Glucose 134-141 thymoma viral proto-oncogene 1 Mus musculus 104-107 34053181-3 2021 Akt2-KO mice exhibited symptoms of DCM (cardiac remodelling and dysfunction), and reduced expression of glycogen and glucose metabolism-related proteins, despite an increase in total Akt (t-Akt) phosphorylation. Glucose 117-124 thymoma viral proto-oncogene 1 Mus musculus 0-3 33660027-4 2021 In streptozotocin-induced T1DM mice, Li/low-dose insulin facilitates glucose uptake through increase the level of exocyst complex component 7 (Exoc7) and Ser473-AKT. Glucose 69-76 thymoma viral proto-oncogene 1 Mus musculus 161-164 33537812-0 2021 FBXW7 mediates high glucose-induced SREBP-1 expression in renal tubular cells of diabetic nephropathy under PI3K/Akt pathway regulation. Glucose 20-27 thymoma viral proto-oncogene 1 Mus musculus 113-116 33537812-11 2021 It was found that the PI3K/Akt signaling pathway was activated in high glucose-stimulated HKC cells, and inhibition of PI3K/Akt pathway using LY294002 increased FBXW7 expression and decreased SREBP-1 expression. Glucose 71-78 thymoma viral proto-oncogene 1 Mus musculus 27-30 33537812-12 2021 Taken together, the present results suggested that FBXW7 mediated high glucose-induced SREBP-1 expression in renal tubular cells of DN, under the regulation of the PI3K/Akt signaling pathway. Glucose 71-78 thymoma viral proto-oncogene 1 Mus musculus 169-172 33795530-6 2021 ROS-induced activation of phosphatase and tensin homolog (PTEN)/ protein kinase B (AKT) signaling after PBMT promoted glucose transporter GLUT4 translocation and glycogen synthase (GS) activation, accelerating glucose uptake and glycogen synthesis in skeletal muscle. Glucose 118-125 thymoma viral proto-oncogene 1 Mus musculus 83-86 33795530-6 2021 ROS-induced activation of phosphatase and tensin homolog (PTEN)/ protein kinase B (AKT) signaling after PBMT promoted glucose transporter GLUT4 translocation and glycogen synthase (GS) activation, accelerating glucose uptake and glycogen synthesis in skeletal muscle. Glucose 210-217 thymoma viral proto-oncogene 1 Mus musculus 83-86 33516878-0 2021 Perilipin 5 ameliorates high-glucose-induced podocyte injury via Akt/GSK-3beta/Nrf2-mediated suppression of apoptosis, oxidative stress, and inflammation. Glucose 29-36 thymoma viral proto-oncogene 1 Mus musculus 65-68 33613705-0 2021 4-Methoxybenzylalcohol protects brain microvascular endothelial cells against oxygen-glucose deprivation/reperfusion-induced injury via activation of the PI3K/AKT signaling pathway. Glucose 85-92 thymoma viral proto-oncogene 1 Mus musculus 159-162 33295913-5 2021 Furthermore, in 3T3-L1 pre-adipocytes, high levels of glucose induced thioredoxin interacting protein (TXNIP) expression and activated the NLRP3 inflammasome, which was counteracted by docosahexaenoic acid (DHA), the major n-3 PUFA in fat-1 mice, by downregulating TXNIP via the phosphatidylinositol-3-kinase (PI3K)/Akt pathway. Glucose 54-61 thymoma viral proto-oncogene 1 Mus musculus 316-319 33337347-0 2021 Hypothalamic BMP9 suppresses glucose production by central PI3K/Akt /mTOR pathway. Glucose 29-36 thymoma viral proto-oncogene 1 Mus musculus 64-67 33647469-12 2021 Increased inhibition of lipolysis may be attributed to increased vascularization in white AT, while increased glucose uptake in BAT was associated with increased Akt phosphorylation and P38/JNK de-phosphorylation. Glucose 110-117 thymoma viral proto-oncogene 1 Mus musculus 162-165 32749748-4 2021 AUR improves glucose by activating the expression of PI3K, Akt and GLUT4, GLUT2. Glucose 13-20 thymoma viral proto-oncogene 1 Mus musculus 59-62 33414476-5 2021 Furthermore, HDAC5 expression was regulated by PI3K/Akt signaling pathway and inhibition of PI3K/Akt pathway by LY294002 treatment or Akt phosphorylation mutation reduced HDAC5 and TGF-beta1 expression in vitro high glucose-cultured HK2 cells. Glucose 216-223 thymoma viral proto-oncogene 1 Mus musculus 52-55 33414476-5 2021 Furthermore, HDAC5 expression was regulated by PI3K/Akt signaling pathway and inhibition of PI3K/Akt pathway by LY294002 treatment or Akt phosphorylation mutation reduced HDAC5 and TGF-beta1 expression in vitro high glucose-cultured HK2 cells. Glucose 216-223 thymoma viral proto-oncogene 1 Mus musculus 97-100 33414476-5 2021 Furthermore, HDAC5 expression was regulated by PI3K/Akt signaling pathway and inhibition of PI3K/Akt pathway by LY294002 treatment or Akt phosphorylation mutation reduced HDAC5 and TGF-beta1 expression in vitro high glucose-cultured HK2 cells. Glucose 216-223 thymoma viral proto-oncogene 1 Mus musculus 97-100 32942336-10 2021 Inhibition of PI3K/AKT/mTOR signalling with LY294002 activated autophagy in clusterin-overexpressing GC-1 spg cells under high glucose conditions. Glucose 127-134 thymoma viral proto-oncogene 1 Mus musculus 19-22 32816106-7 2021 RESULTS: By examining a potential feedback loop, we found decreased phosphorylation of MST1 and Lats1 and increased PI3K/Akt activation in db/db mice and high glucose-treated MCs, along with increased MC proliferation. Glucose 159-166 thymoma viral proto-oncogene 1 Mus musculus 121-124 32615095-11 2020 After the addition of AKT activator to cultures of Per2-overexpressed OSCC cells, reduced glucose uptake, lactic acid production, and cell proliferation, combined with increased apoptosis, were substantially reversed. Glucose 90-97 thymoma viral proto-oncogene 1 Mus musculus 22-25 33287820-8 2020 RESULTS: Here we show that insulin-stimulated phosphorylation of mitochondrial Akt is a prerequisite for transducing insulin"s direct stimulation of glucose oxidation. Glucose 149-156 thymoma viral proto-oncogene 1 Mus musculus 79-82 33287820-9 2020 Inhibition of mitochondrial Akt completely abolishes insulin-stimulated glucose oxidation, independent of glucose uptake or glycolysis. Glucose 72-79 thymoma viral proto-oncogene 1 Mus musculus 28-31 33287820-13 2020 CONCLUSION: We identify, for the first time, insulin-stimulated mitochondrial Akt as a prerequisite transmitter of the insulin signal that directly stimulates cardiac glucose oxidation. Glucose 167-174 thymoma viral proto-oncogene 1 Mus musculus 78-81 33262292-4 2020 In wild-type mice, metabolic reactions were rapidly regulated within 10 min of oral glucose administration by glucose-responsive metabolites, which functioned as allosteric regulators and substrates of metabolic enzymes, and by Akt-induced changes in the expression of glucose-responsive genes encoding metabolic enzymes. Glucose 84-91 thymoma viral proto-oncogene 1 Mus musculus 228-231 32888158-10 2020 miR-204 inhibitors could also suppress high-glucose-induced inflammation in 3T3-L1 cells via promoting SIRT1/ GLUT4/PPARgamma/AKT pathway. Glucose 44-51 thymoma viral proto-oncogene 1 Mus musculus 126-129 32827692-7 2020 Moreover, HGF treatment obviously prevented inactivation of the protein kinase B (Akt)-glycogen synthase kinase 3 beta (GSK3beta)-transcription factor EB (TFEB) axis in high glucose-stimulated podocytes, which was associated with improved lysosome function and autophagy. Glucose 174-181 thymoma viral proto-oncogene 1 Mus musculus 82-85 32512010-0 2020 High glucose-induced ROS accumulation is a critical regulator of ERK1/2-Akt-tuberin-mTOR signalling in RGC-5 cells. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 72-75 33061888-8 2020 Results: vitro, WS-PE increased glucose uptake by stimulating GLUT4 expression and translocation, which were regulated by Akt phosphorylation. Glucose 32-39 thymoma viral proto-oncogene 1 Mus musculus 122-125 32911464-8 2020 In conclusion, LNK plays a pivotal role in adipose glucose transport by regulating insulin-mediated IRS1/PI3K/Akt/AS160 signaling. Glucose 51-58 thymoma viral proto-oncogene 1 Mus musculus 110-113 32450527-0 2020 Apelin-13 attenuates high glucose-induced calcification of MOVAS cells by regulating MAPKs and PI3K/AKT pathways and ROS-mediated signals. Glucose 26-33 thymoma viral proto-oncogene 1 Mus musculus 100-103 32842637-11 2020 Further, the phosphorylation of AKT, a main metabolic sensor activated by insulin in the liver, was enhanced only in the DHT group, which was the only PCOS model showing glucose intolerance and AKT dephosphorylation. Glucose 170-177 thymoma viral proto-oncogene 1 Mus musculus 32-35 32450527-8 2020 Moreover, apelin-13 also effectively improved high glucose-induced dysfunction of MAPKs and PI3K/AKT. Glucose 51-58 thymoma viral proto-oncogene 1 Mus musculus 97-100 32714403-0 2020 Antidiabetic Effects of Arginyl-Fructosyl-Glucose, a Nonsaponin Fraction from Ginseng Processing in Streptozotocin-Induced Type 2 Diabetic Mice through Regulating the PI3K/AKT/GSK-3beta and Bcl-2/Bax Signaling Pathways. Glucose 42-49 thymoma viral proto-oncogene 1 Mus musculus 172-175 32640667-0 2020 Asaronic Acid Inhibited Glucose-Triggered M2-Phenotype Shift Through Disrupting the Formation of Coordinated Signaling of IL-4Ralpha-Tyk2-STAT6 and GLUT1-Akt-mTOR-AMPK. Glucose 24-31 thymoma viral proto-oncogene 1 Mus musculus 154-157 32661238-5 2020 Further, mir-20a-5p could inhibit the expression of PTEN and ATG7 in EPCs, and promote the phosphorylation of AKT and mTOR proteins under high-glucose condition. Glucose 143-150 thymoma viral proto-oncogene 1 Mus musculus 110-113 32661238-7 2020 Circ-ADAM9 upregulated PTEN and ATG7 in interaction with mir-20a-5p, and inhibited the phosphorylation of AKT and mTOR to aggravate autophagy and apoptosis of EPCs under high glucose. Glucose 175-182 thymoma viral proto-oncogene 1 Mus musculus 106-109 32733280-9 2020 Moreover, Se-SP dramatically attenuated high glucose-induced dysfunction of mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3-kinase/AKT (PI3K/AKT) pathways. Glucose 45-52 thymoma viral proto-oncogene 1 Mus musculus 152-155 32733280-9 2020 Moreover, Se-SP dramatically attenuated high glucose-induced dysfunction of mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3-kinase/AKT (PI3K/AKT) pathways. Glucose 45-52 thymoma viral proto-oncogene 1 Mus musculus 162-165 32640667-10 2020 These results demonstrated that asaronic acid allayed glucose-activated M2-phenotype shift through disrupting coordinated signaling of IL-4Ralpha-Tyk2-STAT6 in parallel with GLUT1-Akt-mTOR-AMPK pathway. Glucose 54-61 thymoma viral proto-oncogene 1 Mus musculus 180-183 32197570-4 2020 The presence of bound phenolics interventions could activate the IRS1/AKT/GLUT4 insulin signaling pathway in skeletal muscle, and alter gut microbiota by modulating gut microbiota dysbiosis and enriching the butyric acid-producing bacteria genera of the families Lachnospiraceae and Ruminococcaceae, thus lead to the reduction of blood glucose levels. Glucose 336-343 thymoma viral proto-oncogene 1 Mus musculus 70-73 32325423-7 2020 Moreover, SRT1720 regulates PDH-related glucose oxidative metabolism to reduce NLRP3 inflammasome activation and pyroptosis in an Akt signaling dependent manner during I/R. Glucose 40-47 thymoma viral proto-oncogene 1 Mus musculus 130-133 31585505-9 2019 Additionally, Acads-deficient mice displayed significantly higher expression of the endoplasmic chaperone 78-kDa glucose-regulated protein, which was further associated with the AKT activation in the primary hepatocytes. Glucose 113-120 thymoma viral proto-oncogene 1 Mus musculus 178-181 32271168-5 2020 At the cellular level, sPRR-His enhanced insulin-induced increases in glucose uptake via upregulation of phosphorylated AKT and protein abundance of glucose transporter 4. Glucose 70-77 thymoma viral proto-oncogene 1 Mus musculus 120-123 31735337-0 2020 PICK1 attenuates high glucose-induced pancreatic beta-cell death through the PI3K/Akt pathway and is negatively regulated by miR-139-5p. Glucose 22-29 thymoma viral proto-oncogene 1 Mus musculus 82-85 32133736-4 2020 DUB screening platform identified USP1 as a direct DUB for Akt, and USP1 depletion in mouse muscle increased Akt ubiquitination, PI3K-Akt-FoxO signaling, and glucose uptake during fasting. Glucose 158-165 thymoma viral proto-oncogene 1 Mus musculus 59-62 31887379-0 2020 Exopolysaccharides of Bacillus amyloliquefaciens modulate glycemic level in mice and promote glucose uptake of cells through the activation of Akt. Glucose 93-100 thymoma viral proto-oncogene 1 Mus musculus 143-146 31887379-9 2020 The enhanced glucose uptake of cells was likely mediated by the activation of phosphatidylinositol-3-kinase and Akt and was independent of insulin receptor substrate and AMP-activated protein kinase. Glucose 13-20 thymoma viral proto-oncogene 1 Mus musculus 112-115 31680298-0 2020 LncRNA-XIST/microRNA-126 sponge mediates cell proliferation and glucose metabolism through the IRS1/PI3K/Akt pathway in glioma. Glucose 64-71 thymoma viral proto-oncogene 1 Mus musculus 105-108 32148419-12 2020 Moreover, we found that KGC05P0 regulated glucose production by down-regulation of the PI3K/AKT pathway, which inhibited gluconeogenesis. Glucose 42-49 thymoma viral proto-oncogene 1 Mus musculus 92-95 31634780-0 2019 High glucose inhibits myogenesis and induces insulin resistance by down-regulating AKT signaling. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 83-86 31634780-7 2019 AKT activator SC79 and inhibitor MK2206 was utilized to reveal the important role of AKT signaling in myogenesis and insulin sensitivity inhibited by high glucose. Glucose 155-162 thymoma viral proto-oncogene 1 Mus musculus 0-3 31634780-7 2019 AKT activator SC79 and inhibitor MK2206 was utilized to reveal the important role of AKT signaling in myogenesis and insulin sensitivity inhibited by high glucose. Glucose 155-162 thymoma viral proto-oncogene 1 Mus musculus 85-88 31634780-9 2019 The influences of high glucose on myogenesis and IR was related to decreased AKT activation. Glucose 23-30 thymoma viral proto-oncogene 1 Mus musculus 77-80 31634780-12 2019 CONCLUSION: The present study reveals that high glucose inhibited myogenisis accompanied by inducing IR, through AKT signaling inhibition, which may help to further research for resisting degenerative muscular diseases caused by glucose metabolism disorders. Glucose 48-55 thymoma viral proto-oncogene 1 Mus musculus 113-116 29111280-5 2019 Akt/PKB is capable of inducing a great number of downstream molecules, such as translocating glucose transporters GLUTs to the cell membrane thus increase glucose uptake. Glucose 93-100 thymoma viral proto-oncogene 1 Mus musculus 0-3 31327153-6 2019 In the process of inhibiting Akt, PMA-activated PKC decreased downstream insulin signalling proteins like Akt substrate 160 kDa (AS160) and glycogen synthase kinase (GSK3beta), followed by a decrease of glucose uptake in N2a cells. Glucose 203-210 thymoma viral proto-oncogene 1 Mus musculus 29-32 31032949-9 2019 High glucose inhibited p-AKT production and B-Cell CLL/Lymphoma 2 expression, and promoted BAX and caspase-3 expression. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 25-28 31032949-11 2019 An AKT inhibitor enhanced the effects of high glucose. Glucose 46-53 thymoma viral proto-oncogene 1 Mus musculus 3-6 29111280-5 2019 Akt/PKB is capable of inducing a great number of downstream molecules, such as translocating glucose transporters GLUTs to the cell membrane thus increase glucose uptake. Glucose 93-100 thymoma viral proto-oncogene 1 Mus musculus 4-7 29111280-5 2019 Akt/PKB is capable of inducing a great number of downstream molecules, such as translocating glucose transporters GLUTs to the cell membrane thus increase glucose uptake. Glucose 155-162 thymoma viral proto-oncogene 1 Mus musculus 0-3 29111280-5 2019 Akt/PKB is capable of inducing a great number of downstream molecules, such as translocating glucose transporters GLUTs to the cell membrane thus increase glucose uptake. Glucose 155-162 thymoma viral proto-oncogene 1 Mus musculus 4-7 31562809-0 2019 MiR-27a promotes insulin resistance and mediates glucose metabolism by targeting PPAR-gamma-mediated PI3K/AKT signaling. Glucose 49-56 thymoma viral proto-oncogene 1 Mus musculus 106-109 31241545-0 2019 Concentrate Growth Factors Regulate Osteogenic Dysfunction of MC3T3-E1 Cells Induced by High Glucose Through PI3K/Akt Signaling Pathway. Glucose 93-100 thymoma viral proto-oncogene 1 Mus musculus 114-117 31241545-8 2019 CONCLUSIONS: It was concluded that the soluble factors released by CGF could significantly attenuate high glucose-mediated MC3T3-E1 cells osteogenic dysfunction through the PI3K/Akt pathway. Glucose 106-113 thymoma viral proto-oncogene 1 Mus musculus 178-181 31814568-0 2019 [Chronic high glucose inhibits AKT phosphorylation and promotes M1 polarization of mouse RAW264.7 macrophages]. Glucose 14-21 thymoma viral proto-oncogene 1 Mus musculus 31-34 31814568-10 2019 Conclusion Chronic high glucose induces macrophages to transform into pro-inflammatory M1 type and the continuous chronic inflammatory response, which may be related to the inhibition of AKT protein phosphorylation. Glucose 24-31 thymoma viral proto-oncogene 1 Mus musculus 187-190 31755338-3 2019 Glucose enhances cell apoptosis mediated through PI3K/Akt, ERK1/2, and Bax/Bcl-2 pathways. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 54-57 31755338-8 2019 Incubation of DCs with high glucose significantly decreased A20 protein expression in both control and Akt1-silenced DCs, but not in Akt2-/- DCs. Glucose 28-35 thymoma viral proto-oncogene 1 Mus musculus 103-107 31444134-4 2019 Since the skeletal muscle accounts for a significant amount of postprandial glucose disposal, a popular hypothesis in the diabetes field suggests that a reduction in Akt, specifically in skeletal muscle, leads to systemic glucose intolerance and insulin resistance. Glucose 76-83 thymoma viral proto-oncogene 1 Mus musculus 166-169 31444134-8 2019 RESULTS: Surprisingly, mice lacking Akt2 alone in skeletal muscle displayed normal skeletal muscle insulin signaling, glucose tolerance, and insulin sensitivity despite a dramatic reduction in phosphorylated Akt. Glucose 118-125 thymoma viral proto-oncogene 1 Mus musculus 36-39 31444134-13 2019 Mechanistically, chronic ablation of Akt induced mitochondrial dysfunction and activation of AMPK, which was required for insulin-stimulated glucose uptake in the absence of Akt. Glucose 141-148 thymoma viral proto-oncogene 1 Mus musculus 37-40 31562809-8 2019 miR-27a is considered to be involved in the PPAR-gamma-PI3K/AKT-GLUT4 signaling axis, thus leading to increased glucose uptake and decreased IR in HFD-fed mice and 3T3-L1 adipocytes. Glucose 112-119 thymoma viral proto-oncogene 1 Mus musculus 60-63 30919745-0 2019 Phenethyl isothiocyanate stimulates glucose uptake through the Akt pathway in C2C12 myotubes. Glucose 36-43 thymoma viral proto-oncogene 1 Mus musculus 63-66 31391499-7 2019 In contrast, the diabetic BMDMs cultured under high glucose conditions presented increased levels of lactate and reduced phosphorylation of AKT, PKC-delta and p46 SAPK/JNK but enhanced phosphorylation of the p46 subunit of SAPK/JNK after LPS stimulation. Glucose 52-59 thymoma viral proto-oncogene 1 Mus musculus 140-143 31268904-0 2019 Metformin improved oxidized low-density lipoprotein-impaired mitochondrial function and increased glucose uptake involving Akt-AS160 pathway in raw264.7 macrophages. Glucose 98-105 thymoma viral proto-oncogene 1 Mus musculus 123-126 31268904-11 2019 Moreover, metformin-mediated Akt activation increased Akt substrate of 160 kDa (AS160) phosphorylation (0.51 +- 0.04 vs. 1.03 +- 0.03, P = 0.0041), promoted membrane translocation of glucose transporter 1, and increased glucose influx into the cells (4.78 +- 0.04 vs. 5.47 +- 0.01, P < 0.001). Glucose 183-190 thymoma viral proto-oncogene 1 Mus musculus 29-32 30980919-6 2019 Moreover, other DGK isozymes, DGKeta and zeta, as well as glucose uptake-related proteins, such as protein kinase C (PKC) alpha, PKCzeta, Akt and glycogen synthase kinase 3beta, failed to be stabilized by myristic acid. Glucose 58-65 thymoma viral proto-oncogene 1 Mus musculus 138-141 30919745-6 2019 Inhibition of Akt suppressed PEITC-induced Glut4 translocation and glucose uptake, whereas ERK inhibition did not. Glucose 67-74 thymoma viral proto-oncogene 1 Mus musculus 14-17 30919745-9 2019 These results indicate that PEITC promotes glucose utilization through the ErbB/Akt pathway in C2C12 myotubes. Glucose 43-50 thymoma viral proto-oncogene 1 Mus musculus 80-83 30742994-7 2019 More importantly, in addition to these direct anti-obesity activities, celastrol augmented the PGC-1alpha and GLUT4 expression in adipocytes and skeletal muscles to increase glucose uptake through AKT and P38 MAPK activation. Glucose 174-181 thymoma viral proto-oncogene 1 Mus musculus 197-200 30515796-5 2019 Currently, we found that NEAT1 was greatly upregulated in DM rats and glucose-induced mice mesangial cells, in which a high activation of Akt/mTOR signaling was also observed. Glucose 70-77 thymoma viral proto-oncogene 1 Mus musculus 138-141 30888860-1 2019 Akt is a critical mediator of insulin-stimulated glucose uptake in skeletal muscle. Glucose 49-56 thymoma viral proto-oncogene 1 Mus musculus 0-3 30796916-11 2019 The findings in myotubes can be explained by diminished activation of Akt/PKB by mTORC2 and downstream effects on GSK3beta, impairing the translocation of GLUT4 and the uptake of glucose. Glucose 179-186 thymoma viral proto-oncogene 1 Mus musculus 70-77 30835511-7 2019 Glucose transport protein-3 and fatty acid binding protein-4 were downregulated with reducing GPR1 in vivo and in vitro via phosphorylated AKT pathway. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 139-142 30720225-8 2019 Increased glucose uptake, punctate pattern of GLUT-1 localization, and intracellular pyruvate levels resulting from BITC exposure were significantly attenuated in the presence of a pharmacological inhibitor of AKT (MK-2206). Glucose 10-17 thymoma viral proto-oncogene 1 Mus musculus 210-213 30913518-8 2019 Moreover, Nrf2 knockdown increased the Glu4 protein level and decreased AKT and GSK3beta protein phosphorylation in M1 macrophages, suggesting multiple roles for Nrf2 in regulating glucose metabolism in macrophages. Glucose 181-188 thymoma viral proto-oncogene 1 Mus musculus 72-75 30720225-11 2019 These results indicate increased glucose uptake/metabolism by BITC treatment in breast cancer cells suggesting that breast cancer chemoprevention by BITC may be augmented by pharmacological inhibition of AKT. Glucose 33-40 thymoma viral proto-oncogene 1 Mus musculus 204-207 30604460-11 2019 As a consequence of anti-ER stress, the activation of ACE2 led to improved glucose and lipid metabolism through the IKKbeta/NFkappaB/IRS1/Akt pathway. Glucose 75-82 thymoma viral proto-oncogene 1 Mus musculus 138-141 31275971-7 2019 Quantitative real-time PCR, Western blotting, and immunofluorescence staining revealed that high glucose induced ROS levels and podocytes apoptosis were downregulated by PI3K/AKT and Nrf2 signaling pathways. Glucose 97-104 thymoma viral proto-oncogene 1 Mus musculus 175-178 30914477-4 2019 Here we explored the role of csGRP78 in regulating high glucose (HG)-induced profibrotic AKT Ser/Thr kinase (AKT) signaling and up-regulation of extracellular matrix proteins. Glucose 56-63 thymoma viral proto-oncogene 1 Mus musculus 89-92 30914477-4 2019 Here we explored the role of csGRP78 in regulating high glucose (HG)-induced profibrotic AKT Ser/Thr kinase (AKT) signaling and up-regulation of extracellular matrix proteins. Glucose 56-63 thymoma viral proto-oncogene 1 Mus musculus 109-112 30526118-8 2019 Finally, the study demonstrated that improved glucose metabolism by rAAV-MPRO pretreatment might be due to the activation of the PI3K/Akt/GSK3beta pathway and spurring Glut4 transposition from the cytoplasm to the cytomembrane in C2C12 cells. Glucose 46-53 thymoma viral proto-oncogene 1 Mus musculus 134-137 30626440-7 2019 The increase in insulin stimulated glucose oxidation was accompanied by activation of the IRS-1/Akt/AS160/GSK-3beta pathway, an increase in GLUT4 expression and a reduction in pyruvate dehydrogenase phosphorylation. Glucose 35-42 thymoma viral proto-oncogene 1 Mus musculus 96-99 30362584-0 2019 Prolonged high-glucose exposure decreased SREBP-1/FASN/ACC in Schwann cells of diabetic mice via blocking PI3K/Akt pathway. Glucose 15-22 thymoma viral proto-oncogene 1 Mus musculus 111-114 30650995-0 2019 Alizarin increase glucose uptake through PI3K/Akt signaling and improve alloxan-induced diabetic mice. Glucose 18-25 thymoma viral proto-oncogene 1 Mus musculus 46-49 29975570-4 2019 Mouse proximal tubular cells exposed to high glucose showed significant increase in phosphorylation of Akt and Gal-1. Glucose 45-52 thymoma viral proto-oncogene 1 Mus musculus 103-106 28502041-3 2018 Our findings showed that the glucose administration increased phosphorylated Akt, phosphorylated CREB, exon 1- and exon 4-specific BDNF transcripts, and FGF1 transcripts that are associated with the epigenetic changes expected to open the chromatin and a reduction in histone deacetylase 2 (HDAC2) in neurons and astrocytes of the murine hippocampus. Glucose 29-36 thymoma viral proto-oncogene 1 Mus musculus 77-80 30168649-0 2018 TXNIP regulates AKT-mediated cellular senescence by direct interaction under glucose-mediated metabolic stress. Glucose 77-84 thymoma viral proto-oncogene 1 Mus musculus 16-19 30168649-7 2018 In addition, we found that TXNIP interacted with AKT via the PH domain of AKT, and their interaction was increased by high glucose or H2 O2 treatment. Glucose 123-130 thymoma viral proto-oncogene 1 Mus musculus 49-52 30168649-7 2018 In addition, we found that TXNIP interacted with AKT via the PH domain of AKT, and their interaction was increased by high glucose or H2 O2 treatment. Glucose 123-130 thymoma viral proto-oncogene 1 Mus musculus 74-77 30168649-11 2018 Altogether, these results suggest that TXNIP regulates cellular senescence by inhibiting AKT pathways via a direct interaction under conditions of glucose-derived metabolic stress. Glucose 147-154 thymoma viral proto-oncogene 1 Mus musculus 89-92 30031227-9 2018 In parallel, we analysed the O-GlcNAcylation/phosphorylation ratio of IRS1 and AKT, whose alterations may contribute to insulin resistance and reduced glucose uptake. Glucose 151-158 thymoma viral proto-oncogene 1 Mus musculus 79-82 30118770-10 2018 The in vitro experimental results showed that both catalpol and metformin enhanced glucose uptake via activation of PI3K/AKT pathway. Glucose 83-90 thymoma viral proto-oncogene 1 Mus musculus 121-124 29486284-0 2018 Herpud1 impacts insulin-dependent glucose uptake in skeletal muscle cells by controlling the Ca2+-calcineurin-Akt axis. Glucose 34-41 thymoma viral proto-oncogene 1 Mus musculus 110-113 30775979-7 2019 Since the PI3K/AKT pathway affects several downstream targets associated with metabolism (e.g., GSK3, glucose transporters), western blots were used to examine possible alterations in the expression, translocation, or activation of these targets. Glucose 102-109 thymoma viral proto-oncogene 1 Mus musculus 15-18 30231545-6 2018 This was accompanied by significantly increased activation levels of the glucose metabolism regulators 160 kDa AKT substrate (AS160), 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2), and glycogen synthase kinase-3beta (GSK3beta). Glucose 73-80 thymoma viral proto-oncogene 1 Mus musculus 111-114 29605032-9 2018 RESULTS: Diabetic mice or H9c2 cells exposed to high glucose displayed a larger infarct size, more severe cardiomyocyte apoptosis, lower cell viability, and increased oxidative stress, which were associated with increased levels of PHLPP-1 and reduced levels of p-Akt and nuclear factor-erythroid-2-related factor 2 (Nrf2) protein expression. Glucose 53-60 thymoma viral proto-oncogene 1 Mus musculus 264-267 28926104-9 2018 Glucose activated Akt/HIF-1alpha signaling pathway, which might be at least in part responsible for glucose-induced glycolysis and cell proliferation. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 18-21 28926104-9 2018 Glucose activated Akt/HIF-1alpha signaling pathway, which might be at least in part responsible for glucose-induced glycolysis and cell proliferation. Glucose 100-107 thymoma viral proto-oncogene 1 Mus musculus 18-21 29203232-7 2018 Knockdown of TXNIP suppressed moderately high glucose (MHG)-induced reactive oxygen species (ROS) generation, migration, tube formation and activation of Akt/mTOR pathway in HRMECs. Glucose 46-53 thymoma viral proto-oncogene 1 Mus musculus 154-157 28851713-3 2018 During glucose synthesis, the activity of FoxO1/3a is negatively regulated by Akt-mediated phosphorylation, which leads to the cytoplasmic retention of FoxO1/3a. Glucose 7-14 thymoma viral proto-oncogene 1 Mus musculus 78-81 28866332-1 2017 Previously 10 muM permethrin (38.7% cis and 59.4% trans isomers), a pyrethroid insecticide widely used in agriculture and household products for pest control, was reported to reduce insulin-stimulated glucose uptake and phosphorylation of protein kinase B (p-AKT) in C2C12 mouse myotubes. Glucose 201-208 thymoma viral proto-oncogene 1 Mus musculus 259-262 29204135-3 2017 We tested the hypothesis that ucOC per se stimulates muscle glucose uptake via extracellular signal-regulated kinase (ERK), adenosine monophosphate-activated protein kinase (AMPK), and/or the mechanistic target of rapamycin complex 2 (mTORC2)-protein kinase B (AKT)-AKT substrate of 160 kDa (AS160) signaling cascade. Glucose 60-67 thymoma viral proto-oncogene 1 Mus musculus 261-264 28874678-10 2017 In summary, loss of mitochondrial CypD results in a shift in bioenergetics and in activation of glucose-metabolism regulating Akt/AMPK/p70S6 kinase pathways that is expected to affect the capability of Ppif-/- mice kidneys to react to stimuli and injury. Glucose 96-103 thymoma viral proto-oncogene 1 Mus musculus 126-129 28607454-2 2017 Adenovirus 36 (Ad36) infection can increase the uptake of excess glucose from blood into adipocytes by increasing GLUT4 translocation through the Ras-Akt signaling pathway, which bypasses PI3K-Akt-mediated insulin receptor signaling. Glucose 65-72 thymoma viral proto-oncogene 1 Mus musculus 150-153 27791278-12 2017 Enhancement of GLUT4 and phospho Akt protein expression seems to be responsible for the increment in glucose uptake and enhanced insulin signaling, respectively. Glucose 101-108 thymoma viral proto-oncogene 1 Mus musculus 33-36 28498916-2 2017 We tested the postnatal expression of Akt-unresponsive, constitutively active mutants of three major Akt substrates widely considered to regulate glucose metabolism [i.e., FoxO1, PGC1alpha, and glycogen synthase kinase-3beta (GSK3beta)] using adenoviral gene delivery to the mouse liver. Glucose 146-153 thymoma viral proto-oncogene 1 Mus musculus 101-104 28424212-0 2017 PDGF receptor-beta uses Akt/mTORC1 signaling node to promote high glucose-induced renal proximal tubular cell collagen I (alpha2) expression. Glucose 66-73 thymoma viral proto-oncogene 1 Mus musculus 24-27 28424212-7 2017 We also found that PDGFRbeta regulates high glucose-induced Akt activation, its targets tuberin and PRAS40 phosphorylation, and finally, mTORC1 activation. Glucose 44-51 thymoma viral proto-oncogene 1 Mus musculus 60-63 28424212-13 2017 Our results identify PDGFRbeta as a driver in activating Akt/mTORC1 nexus for high glucose-mediated expression of collagen I (alpha2) in proximal tubular epithelial cells, which contributes to tubulointerstitial fibrosis in diabetic nephropathy. Glucose 83-90 thymoma viral proto-oncogene 1 Mus musculus 57-60 28246289-7 2017 In conclusion, the FAM3C-HSF1-CaM-Akt pathway plays important roles in regulating glucose and lipid metabolism in hepatocytes independent of insulin and calcium. Glucose 82-89 thymoma viral proto-oncogene 1 Mus musculus 34-37 28075049-9 2017 In summary, our study suggests that decreased SHIP mediates high glucose-induced TGF-beta1 upregulation and ECM deposition through activation of the PI3K/Akt pathway in renal tubular cells. Glucose 65-72 thymoma viral proto-oncogene 1 Mus musculus 154-157 28292218-0 2017 High glucose induces alternative activation of macrophages via PI3K/Akt signaling pathway. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 68-71 28292218-8 2017 What"s more, Akt was phosphorylated at the eighth hour stimulated by high glucose medium, and LY294002 inhibited the expression of Arg-1 and CD206 by blocking the phosphorylation of Akt. Glucose 74-81 thymoma viral proto-oncogene 1 Mus musculus 13-16 28292218-9 2017 CONCLUSIONS: Our study indicated that high glucose rather than high osmotic pressure induced M2 phenotype via PI3K/Akt signaling pathway. Glucose 43-50 thymoma viral proto-oncogene 1 Mus musculus 115-118 26567247-10 2017 Increased miR-21 expression, decreased PTEN expression and abnormal activation of the PI3K/Akt/mTOR pathway were observed in cells that were cultured in high glucose conditions. Glucose 158-165 thymoma viral proto-oncogene 1 Mus musculus 91-94 28475869-4 2017 Here we identified the Baf60c-Deptor-AKT pathway as a target of muscle glucose sensing that augments insulin action in skeletal myocytes. Glucose 71-78 thymoma viral proto-oncogene 1 Mus musculus 37-40 28475869-6 2017 Mechanistically, glucose triggers KATP channel-dependent calcium signaling, which promotes HDAC5 phosphorylation and nuclear exclusion, leading to Baf60c induction and insulin-independent AKT activation. Glucose 17-24 thymoma viral proto-oncogene 1 Mus musculus 188-191 28075049-5 2017 In vitro research revealed that high glucose-attenuated SHIP expression accompanied the activation of the PI3K/Akt signaling and ECM production. Glucose 37-44 thymoma viral proto-oncogene 1 Mus musculus 111-114 28075049-7 2017 Again, either the M90-SHIP plasmid or the PI3K/Akt pathway inhibitor LY294002 could significantly prevent the high glucose-induced increase in TGF-beta1, alpha-SMA, and secreted Col 3 and decreased E-cadherin. Glucose 115-122 thymoma viral proto-oncogene 1 Mus musculus 47-50 28903400-5 2017 Levels or activities of Src, PDK1, Akt, and NF-kappaB were higher in AGEs- and high glucose-treated cells than those in 3T3-L1 cells. Glucose 84-91 thymoma viral proto-oncogene 1 Mus musculus 35-38 28903400-8 2017 These results suggest that chronic AGEs and high glucose treatments up-regulate Bcl-2 and YAP via the Akt-NF-kappaB pathway and impair adipogenesis. Glucose 49-56 thymoma viral proto-oncogene 1 Mus musculus 102-105 28559971-14 2017 Taken together, our findings suggest that APS promotes glucose uptake and increases insulin sensitivity in 3T3-L1 adipocytes and may involve the miR-721-PPAR-gamma-PI3K/AKT-GLUT4 signaling pathway. Glucose 55-62 thymoma viral proto-oncogene 1 Mus musculus 169-172 27854076-0 2017 Dodeca-2(E),4(E)-dienoic acid isobutylamide enhances glucose uptake in 3T3-L1 cells via activation of Akt signaling. Glucose 53-60 thymoma viral proto-oncogene 1 Mus musculus 102-105 28088384-4 2017 RTC-1-induced inhibition of NADH:ubiquinone oxidoreductase was found to promote glucose uptake in C2C12 myotubes in vitro, through the activation of the Akt substrate of 160kDa (AS160), in response to the increased activity of Akt and AMP-activated protein kinase (AMPK). Glucose 80-87 thymoma viral proto-oncogene 1 Mus musculus 153-156 27903431-0 2017 Differential regulation of baicalin and scutellarin on AMPK and Akt in promoting adipose cell glucose disposal. Glucose 94-101 thymoma viral proto-oncogene 1 Mus musculus 64-67 27903431-7 2017 In contrast, Akt inhibitor and knockdown of Akt with siRNA decreased scutellarin-stimulated glucose uptake but had no effects on baicalin. Glucose 92-99 thymoma viral proto-oncogene 1 Mus musculus 44-47 27854076-4 2017 Additionally, DDI enhanced Akt phosphorylation, whereas phosphoinositide 3-kinase/Akt inhibitors suppressed DDI-induced glucose uptake. Glucose 120-127 thymoma viral proto-oncogene 1 Mus musculus 82-85 27854076-5 2017 These results suggest that DDI may improve insulin sensitivity through the activation of Akt signaling, which leads to enhanced glucose uptake. Glucose 128-135 thymoma viral proto-oncogene 1 Mus musculus 89-92 28373902-9 2017 Akt inhibitor could abolish the beneficial effect of acarbose on high glucose induced EPC dysfunction in vitro, accompanied by reduced eNOS activation. Glucose 70-77 thymoma viral proto-oncogene 1 Mus musculus 0-3 28607575-6 2017 Collectively, these findings suggest that EeSs have a high potentiality to mitigate diabetic symptoms through stimulating glucose uptake in peripheral tissue via the activation of AKT and AMPK signaling cascade and augmenting antioxidant potentiality as well as blocking the gluconeogenesis process in diabetic mice. Glucose 122-129 thymoma viral proto-oncogene 1 Mus musculus 180-183 27634219-6 2016 In vitro, high glucose increases Pin1 expression with an accompanying increase in phospho-Akt (Ser 473), p-Smad2, p-Smad3, TGF-beta1, and alpha-SMA in cardiac fibroblasts (CFs). Glucose 15-22 thymoma viral proto-oncogene 1 Mus musculus 90-93 27521959-4 2016 In glucose responsive tissues like adipose and muscles, activation of Akt is responsible for triggering GLUT4 translocation and glucose transport. Glucose 3-10 thymoma viral proto-oncogene 1 Mus musculus 70-73 27521959-4 2016 In glucose responsive tissues like adipose and muscles, activation of Akt is responsible for triggering GLUT4 translocation and glucose transport. Glucose 128-135 thymoma viral proto-oncogene 1 Mus musculus 70-73 27568038-0 2016 20-HETE attenuates the response of glucose-stimulated insulin secretion through the AKT/GSK-3beta/Glut2 pathway. Glucose 35-42 thymoma viral proto-oncogene 1 Mus musculus 84-87 27497988-7 2016 In vitro experiments, using HK-2 cells, revealed that knockdown of thioredoxin-interacting protein inhibited high glucose-mediated lipid accumulation, expression of acetyl-CoA carboxylase, fatty acid synthase and sterol regulatory element binding protein-1, as well as activation of Akt and mTOR. Glucose 114-121 thymoma viral proto-oncogene 1 Mus musculus 283-286 27784964-8 2016 The expression of glucose glycolysis-related proteins and ECM components decreased remarkably when the PI3K/Akt signaling was blocked by Ly294002 in the activated HSCs. Glucose 18-25 thymoma viral proto-oncogene 1 Mus musculus 108-111 27535223-8 2016 These data suggest insulin acts on beta-cells in an endocrine manner in the normal situation; and that in beta-cells lacking insulin receptors, insulin and glucose minimally activate the Akt pathway, while ERK phosphorylation and FoxO1 nuclear export occur independently of insulin signaling. Glucose 156-163 thymoma viral proto-oncogene 1 Mus musculus 187-190 27746687-6 2016 Inflammatory molecules induced insulin resistance by upregulating phosphorylation of insulin receptor substrate-1 at serine residues and impairing insulin PI3K/Akt signaling, leading to decreased glucose uptake by adipocytes. Glucose 196-203 thymoma viral proto-oncogene 1 Mus musculus 160-163 27251941-1 2016 Insulin facilitates glucose uptake into cells by translocating the glucose transporter GLUT4 towards the cell surface through a pathway along an insulin receptor (IR)/IR substrate 1 (IRS-1)/phosphatidylinositol 3 kinase (PI3K)/3-phosphoinositide-dependent protein kinase-1 (PDK1)/Akt axis. Glucose 20-27 thymoma viral proto-oncogene 1 Mus musculus 280-283 27113027-3 2016 Here we experimentally demonstrate that curcumin inhibited the ubiquitin-proteasome system (UPS) function, activated autophagy, and reduced protein levels of protein kinase B (Akt) in a dose- and time-dependent manner in 3T3-L1 adipocytes, accompanied with attenuation of insulin-stimulated Akt phosphorylation, plasma membrane translocation of glucose transporter type 4 (GLUT4), and glucose uptake. Glucose 345-352 thymoma viral proto-oncogene 1 Mus musculus 176-179 27095850-9 2016 We found that glucose- and H2O2-induced activation of FAK, paxillin, ERK1/2 and Akt was significantly blocked by silencing SCGN. Glucose 14-21 thymoma viral proto-oncogene 1 Mus musculus 80-83 27166156-5 2016 Furthermore, high glucose decreases CTMP expression accompanied by enhanced phospho-Akt (Ser 473), TGF-beta1 and alpha-SMA in cultured human renal proximal tubular epithelial cells (HKC), which are effectively prevented by transfection of pYr-ads-4-musCTMP vector. Glucose 18-25 thymoma viral proto-oncogene 1 Mus musculus 84-87 27669565-0 2016 Suppression of Very Early Stage Of Adipogenesis by Baicalein, a Plant-Derived Flavonoid through Reduced Akt-C/EBPalpha-GLUT4 Signaling-Mediated Glucose Uptake in 3T3-L1 Adipocytes. Glucose 144-151 thymoma viral proto-oncogene 1 Mus musculus 104-107 27019188-6 2016 In addition, miR-20a-5p mimic could reverse high glucose-induced impaired glycogenesis and AKT/GSK activation in NCTC1469 and Hep1-6 cells. Glucose 49-56 thymoma viral proto-oncogene 1 Mus musculus 91-94 27068641-0 2016 High glucose induces autophagy of MC3T3-E1 cells via ROS-AKT-mTOR axis. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 57-60 27068641-1 2016 In the present study, we investigate the function of ROS-AKT-mTOR axis on the apoptosis, proliferation and autophagy of MC3T3-E1 cells, and the proliferation of MC3T3-E1 cells after autophagy inhibition under high glucose conditions. Glucose 214-221 thymoma viral proto-oncogene 1 Mus musculus 57-60 27068641-12 2016 Expression of p-AKT and p-mTOR proteins were dramatically decreased in high glucose group, and NAC reversed their expression. Glucose 76-83 thymoma viral proto-oncogene 1 Mus musculus 16-19 27068641-15 2016 Our present findings reveal that high glucose affects apoptosis, proliferation and autophagy of MC3T3-E1 cells through ROS-AKT-mTOR axis. Glucose 38-45 thymoma viral proto-oncogene 1 Mus musculus 123-126 26607153-0 2016 Insulin sensitizes FGF21 in glucose and lipid metabolisms via activating common AKT pathway. Glucose 28-35 thymoma viral proto-oncogene 1 Mus musculus 80-83 26453611-7 2016 In a renal proximal tubule cell line, either pharmacologic or genetic inhibition of EGFR, Akt, or CREB blunted YAP expression in response to high-glucose treatment. Glucose 146-153 thymoma viral proto-oncogene 1 Mus musculus 90-93 27090933-8 2016 These results strongly suggest that combination treatment (UA/RSG) activates IRS-PI3-kinase-Akt-dependent signaling pathways to induce GLUT 4 translocation and increases the expression of insulin receptor to improve glucose intolerance. Glucose 216-223 thymoma viral proto-oncogene 1 Mus musculus 92-95 26926143-0 2016 Mitochondrial dysfunction precedes depression of AMPK/AKT signaling in insulin resistance induced by high glucose in primary cortical neurons. Glucose 106-113 thymoma viral proto-oncogene 1 Mus musculus 54-57 26447680-6 2016 Again, in vitro experiment revealed 1.89, 2.18, 1.92, 3.06, 2.06-fold increases of phospho-Akt (Ser 473), phospho-Akt (Thr 308), CTGF, secreted fibronectin, and secreted Col 3 in high glucose-stimulated HKC cells in comparison with normal control cells. Glucose 184-191 thymoma viral proto-oncogene 1 Mus musculus 91-94 27153497-7 2016 This results in disruption of AKT, AMPK, and SREBP signaling, leading to altered insulin, glucose, and lipid metabolism. Glucose 90-97 thymoma viral proto-oncogene 1 Mus musculus 30-33 26562537-8 2016 Our results provide direct evidence for the first time that IL-17A overexpression in the central nervous system does not cause physical and learning disabilities and neuroinflammation and suggest that IL-17A may regulate glucose metabolism through the AKT signaling pathway. Glucose 221-228 thymoma viral proto-oncogene 1 Mus musculus 252-255 26739493-0 2016 Hydrophobic motif site-phosphorylated protein kinase CbetaII between mTORC2 and Akt regulates high glucose-induced mesangial cell hypertrophy. Glucose 99-106 thymoma viral proto-oncogene 1 Mus musculus 80-83 26739493-8 2016 In contrast, inhibition of mTORC2 decreased the phosphorylation of PKCbetaII and Akt, leading to inhibition of PRAS40 phosphorylation and mTORC1 activity and prevented mesangial cell hypertrophy in response to high glucose; expression of constitutively active Akt or mTORC1 restored mesangial cell hypertrophy. Glucose 215-222 thymoma viral proto-oncogene 1 Mus musculus 81-84 26739493-9 2016 Moreover, constitutively active PKCbetaII reversed the inhibition of high glucose-stimulated Akt phosphorylation and mesangial cell hypertrophy induced by suppression of mTORC2. Glucose 74-81 thymoma viral proto-oncogene 1 Mus musculus 93-96 27852130-8 2016 Mechanistic studies suggested that the glucose-lowering effect of AGNE was mediated by the activation of AMP activated protein kinase, Akt, and glycogen synthase kinase-3[Formula: see text]. Glucose 39-46 thymoma viral proto-oncogene 1 Mus musculus 135-138 26772600-0 2016 mTORC2 sustains thermogenesis via Akt-induced glucose uptake and glycolysis in brown adipose tissue. Glucose 46-53 thymoma viral proto-oncogene 1 Mus musculus 34-37 27430917-6 2016 The increased glucose uptake induced by these compounds is associated with activation of AMP-activated protein kinase (AMPK) and PI3K/Akt pathways in these cells. Glucose 14-21 thymoma viral proto-oncogene 1 Mus musculus 134-137 26719856-7 2016 Furthermore, we found that uncarboxylated osteocalcin inhibited PI3K/Akt signaling which was induced by ROS and facilitated the osteogenic differentiation of MC3T3-E1 cells under high glucose conditions. Glucose 184-191 thymoma viral proto-oncogene 1 Mus musculus 69-72 26719856-8 2016 Taken together and to the best of ou knowledge, our results demonstrate for the first time that uncarboxylated osteocalcin inhibits high glucose-induced ROS production and stimulates osteoblastic differentiation by inhibiting the activation of PI3K/Akt in MC3T3-E1 cells. Glucose 137-144 thymoma viral proto-oncogene 1 Mus musculus 249-252 26489764-5 2016 Specifically, first-phase insulin secretion in response to glucose was impaired and this effect was related to altered characteristics of focal adhesion kinase activation modulating signaling through Akt, ERK, beta catenin and cAMP. Glucose 59-66 thymoma viral proto-oncogene 1 Mus musculus 200-203 26053972-10 2016 Insulin-stimulated ERK1/2 phosphorylation was diminished by SP, while phosphorylation of Akt was increased, correlating with increased glucose uptake in response to insulin. Glucose 135-142 thymoma viral proto-oncogene 1 Mus musculus 89-92 26487674-3 2016 However, the role of AKT1 in glucose metabolism is not as clearly defined. Glucose 29-36 thymoma viral proto-oncogene 1 Mus musculus 21-25 26195787-1 2015 The serine-threonine kinase Akt is a key regulator of cell proliferation and survival, glucose metabolism, cell mobility, and tumorigenesis. Glucose 87-94 thymoma viral proto-oncogene 1 Mus musculus 28-31 26584623-7 2015 Thus, glucose is a signaling molecule that regulates myogenesis and muscle regeneration via MLX/IGF2/Akt signaling. Glucose 6-13 thymoma viral proto-oncogene 1 Mus musculus 101-104 26226221-10 2015 KLF14 overexpression in Hepa1-6 cells prevented the inhibition of glucose uptake and Akt phosphorylation induced by high glucose and/or high insulin, or T2DM serum. Glucose 121-128 thymoma viral proto-oncogene 1 Mus musculus 85-88 26081285-3 2015 We hypothesized that increasing PRR reduces autophagy and increases apoptosis of mouse podocytes exposed to high glucose via activation of the PI3K/Akt/mTOR signaling pathway. Glucose 113-120 thymoma viral proto-oncogene 1 Mus musculus 148-151 26081285-13 2015 Based on these data, we conclude that high glucose decreases autophagy and increases apoptosis in mouse podocytes through the PRR/PI3K/Akt/mTOR signaling pathway. Glucose 43-50 thymoma viral proto-oncogene 1 Mus musculus 135-138 25808537-4 2015 We show that IAPP activated Erk1/2 and v-akt murine thymoma viral oncogene homolog 1 (Akt) at the picomolar range (10-100 pM) in mouse pancreatic islets and MIN6 beta cells cultured at low glucose concentrations. Glucose 189-196 thymoma viral proto-oncogene 1 Mus musculus 86-89 26451285-1 2015 By regulating Akt membrane compartmentalization, ClipR-59 modulates adipocyte glucose transport. Glucose 78-85 thymoma viral proto-oncogene 1 Mus musculus 14-17 25560828-3 2015 Western blottings revealed that protein kinase B (AKT)-mediated glucose signaling was down-regulated in diabetic testes and further decreased in FGF21-KO diabetic group both 10 days and 2 months after diabetes onset, reflected by reduced glycogen synthase (GS) kinase (GSK)-3beta phosphorylation and increased GS phosphorylation. Glucose 64-71 thymoma viral proto-oncogene 1 Mus musculus 50-53 25475440-10 2015 Hemin and bilirubin reversed high glucose-induced reductions in Akt and eNOS phosphorylation and NO production. Glucose 34-41 thymoma viral proto-oncogene 1 Mus musculus 64-67 25621554-0 2015 Different concentrations of glucose regulate proliferation and osteogenic differentiation of osteoblasts via the PI3 kinase/Akt pathway. Glucose 28-35 thymoma viral proto-oncogene 1 Mus musculus 124-127 25889508-1 2015 BACKGROUND: Glucose homeostasis is distorted by defects of the PI3K/AKT and AMPK pathways in insulin-sensitive tissues, allowing the accumulation of glucose in the blood. Glucose 149-156 thymoma viral proto-oncogene 1 Mus musculus 68-71 25889508-10 2015 CLE regulated glucose uptake and homeostasis via the PI3K/AKT pathway in myocytes and db/db mice, respectively. Glucose 14-21 thymoma viral proto-oncogene 1 Mus musculus 58-61 25621554-6 2015 Furthermore, these effects were significantly inhibited by PI3K/Akt inhibitor LY294002 at a glucose concentration of 15.5 mM, which was the optimum. Glucose 92-99 thymoma viral proto-oncogene 1 Mus musculus 64-67 25621554-7 2015 CONCLUSIONS: Appropriate high glucose concentration (15.5 mM) can increase osteogenic differentiation by activating PI3K/Akt pathway in MC3T3-E1 cells, but exorbitant high glucose concentrations (25.5 and 35.5 mM) inhibited the biomineralization process. Glucose 30-37 thymoma viral proto-oncogene 1 Mus musculus 121-124 26234354-9 2015 These results suggest that in diabetes the GRK2 inhibitor ameliorates vascular endothelial dysfunction via Akt/eNOS signaling by inhibiting GRK2 activity and enhancing beta-arrestin 2 translocation to the membrane under GPCR or non-GPCR stimulation, thereby contributing to blood pressure- and blood glucose-lowering effects. Glucose 300-307 thymoma viral proto-oncogene 1 Mus musculus 107-110 25749152-5 2015 reduced blood glucose levels significantly and increased the protein expressions of insulin receptor beta, insulin receptor substrate 1, protein kinase B (Akt/PKB), IKKalpha, and IkappaBalpha. Glucose 14-21 thymoma viral proto-oncogene 1 Mus musculus 155-162 24874579-7 2014 NAP treatment reduced the phosphorylation levels of ERK and AKT in cells grown in high glucose. Glucose 87-94 thymoma viral proto-oncogene 1 Mus musculus 60-63 25288788-0 2014 High glucose forces a positive feedback loop connecting Akt kinase and FoxO1 transcription factor to activate mTORC1 kinase for mesangial cell hypertrophy and matrix protein expression. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 56-59 25288788-1 2014 High glucose-induced Akt acts as a signaling hub for mesangial cell hypertrophy and matrix expansion, which are recognized as cardinal signatures for the development of diabetic nephropathy. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 21-24 25288788-3 2014 Here we show Akt-dependent phosphorylation of the transcription factor FoxO1 by high glucose. Glucose 85-92 thymoma viral proto-oncogene 1 Mus musculus 13-16 25288788-4 2014 Phosphorylation-deficient, constitutively active FoxO1 inhibited the high glucose-induced phosphorylation of Akt to suppress the phosphorylation/inactivation of PRAS40 and mTORC1 activity. Glucose 74-81 thymoma viral proto-oncogene 1 Mus musculus 109-112 25288788-10 2014 Moreover, we show that catalase blocks high glucose-stimulated Akt phosphorylation to attenuate the inactivation of FoxO1 and PRAS40, resulting in the inhibition of mTORC1 and mesangial cell hypertrophy and fibronectin and PAI-1 expression. Glucose 44-51 thymoma viral proto-oncogene 1 Mus musculus 63-66 25070263-5 2014 In the present study, it was identified that the activation of AKT and glycogen synthase kinase 3 (GSK-3), and the expression levels of glycogen, were reduced in mouse NCTC 1469 hepatocytes and mouse primary hepatocytes, following exposure to 25 mM glucose for 48 h. Furthermore, it was demonstrated that high glucose levels suppressed the expression of miR-152 in hepatocytes. Glucose 249-256 thymoma viral proto-oncogene 1 Mus musculus 63-66 25070263-5 2014 In the present study, it was identified that the activation of AKT and glycogen synthase kinase 3 (GSK-3), and the expression levels of glycogen, were reduced in mouse NCTC 1469 hepatocytes and mouse primary hepatocytes, following exposure to 25 mM glucose for 48 h. Furthermore, it was demonstrated that high glucose levels suppressed the expression of miR-152 in hepatocytes. Glucose 310-317 thymoma viral proto-oncogene 1 Mus musculus 63-66 25070263-6 2014 In order to further assess the effects of miR-152 on the glucose-induced reduction of glycogen synthesis and activation of AKT and GSK, miR-152 mimic and inhibitor were transfected into the NCTC 1469 cells, respectively. Glucose 57-64 thymoma viral proto-oncogene 1 Mus musculus 123-126 25070263-8 2014 Conversely, upregulation of miR-152 by transfection of an miR-152 mimic reversed the glucose-induced decrease in glycogen synthesis and reduced AKT and GSK phosphorylation in hepatocytes. Glucose 85-92 thymoma viral proto-oncogene 1 Mus musculus 144-147 24819347-2 2014 Since zinc mimics the function of insulin, it may provide benefit to the heart via stimulating Akt-mediated glucose metabolism. Glucose 108-115 thymoma viral proto-oncogene 1 Mus musculus 95-98 25070263-10 2014 In conclusion, to the best of our knowledge, this study was the first to indicate that high glucose impaired the activation of the AKT/GSK pathway and the synthesis of glycogen in mouse hepatocytes, in part through the downregulation of miR-152. Glucose 92-99 thymoma viral proto-oncogene 1 Mus musculus 131-134 25400823-0 2014 MiR-378 overexpression attenuates high glucose-suppressed osteogenic differentiation through targeting CASP3 and activating PI3K/Akt signaling pathway. Glucose 39-46 thymoma viral proto-oncogene 1 Mus musculus 129-132 25400823-6 2014 We also found that under high glucose conditions miR-378 activated the PI3K/Akt signaling pathway and down regulated pro-apoptotic CytC, Apaf-1 and Bax proteins via the PI3K/Akt pathway. Glucose 30-37 thymoma viral proto-oncogene 1 Mus musculus 76-79 25400823-6 2014 We also found that under high glucose conditions miR-378 activated the PI3K/Akt signaling pathway and down regulated pro-apoptotic CytC, Apaf-1 and Bax proteins via the PI3K/Akt pathway. Glucose 30-37 thymoma viral proto-oncogene 1 Mus musculus 174-177 25400823-7 2014 Collectively, these results suggest that miR-378 overexpression attenuates high glucose-suppressed osteogenic differentiation through targeting CASP3 and activating the PI3K/Akt pathway. Glucose 80-87 thymoma viral proto-oncogene 1 Mus musculus 174-177 24976766-0 2014 The Stimulatory Effect of Essential Fatty Acids on Glucose Uptake Involves Both Akt and AMPK Activation in C2C12 Skeletal Muscle Cells. Glucose 51-58 thymoma viral proto-oncogene 1 Mus musculus 80-83 24444370-9 2014 Furthermore, experiments in hepatocarcinoma cells revealed that GdCl3 activated the Akt pathway to promote the phosphorylation of FoxO1 (forkhead box O1), leading to the suppression of gluconeogenesis by reducing the expression of PEPCK and G6Pase and resulting in decreased cellular production of glucose. Glucose 298-305 thymoma viral proto-oncogene 1 Mus musculus 84-87 24885625-0 2014 High glucose increases LPS-induced DC apoptosis through modulation of ERK1/2, AKT and Bax/Bcl-2. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 78-81 24885625-8 2014 CONCLUSIONS: These results suggest that high glucose concentrations might prime dendritic cells for apoptosis induced by LPS in the intestinal tract through upregulating the expression of Bax and downregulating the expression of AKT, ERK and Bcl-2. Glucose 45-52 thymoma viral proto-oncogene 1 Mus musculus 229-232 24821545-6 2014 The potential for glucose utilization was increased by increased glucose transporter 1 (GLUT1), GLUT4 and protein kinase B (AKT) protein expression in insulin-resistant 3T3-L1 cells in response to BSK treatment. Glucose 18-25 thymoma viral proto-oncogene 1 Mus musculus 124-127 24832603-11 2014 Collectively, these data indicate that estradiol promotes glucose metabolism in mTORC1 hyperactive cells through the pentose phosphate pathway via Akt reactivation and G6PD upregulation, thereby enhancing cell survival under oxidative stress. Glucose 58-65 thymoma viral proto-oncogene 1 Mus musculus 147-150 24216610-2 2014 Akt and Rac1 are important regulators of insulin-stimulated glucose uptake in skeletal muscle. Glucose 60-67 thymoma viral proto-oncogene 1 Mus musculus 0-3 24806753-9 2014 CONCLUSION: FAM3A plays crucial roles in the regulation of glucose and lipid metabolism in the liver, where it activates the PI3K-Akt signaling pathway by way of a Ca(2+) /CaM-dependent mechanism. Glucose 59-66 thymoma viral proto-oncogene 1 Mus musculus 130-133 24216610-0 2014 Akt and Rac1 signaling are jointly required for insulin-stimulated glucose uptake in skeletal muscle and downregulated in insulin resistance. Glucose 67-74 thymoma viral proto-oncogene 1 Mus musculus 0-3 24216610-4 2014 Here we delineate how Akt and Rac1 pathways signal to increase glucose transport independently of each other and are simultaneously downregulated in insulin resistant muscle. Glucose 63-70 thymoma viral proto-oncogene 1 Mus musculus 22-25 24216610-8 2014 While individual inhibition of Rac1 or Akt partially decreased insulin-stimulated glucose transport by ~40% and ~60%, respectively, their simultaneous inhibition completely blocked insulin-stimulated glucose transport. Glucose 82-89 thymoma viral proto-oncogene 1 Mus musculus 39-42 24216610-9 2014 LatrunculinB plus Akt inhibition blocked insulin-stimulated glucose uptake, while LatrunculinB had no additive effect on Rac1 inhibition. Glucose 60-67 thymoma viral proto-oncogene 1 Mus musculus 18-21 24216610-11 2014 These findings suggest that Rac1 and Akt regulate insulin-stimulated glucose uptake via distinct parallel pathways, and that insulin-induced Rac1 and Akt signaling are both dysfunctional in insulin resistant muscle. Glucose 69-76 thymoma viral proto-oncogene 1 Mus musculus 37-40 24145125-5 2014 Increasing glucose concentrations elicited a rise in Akt and neuronal nitric oxide synthase (nNOS) phosphorylation, CaMKKbeta levels, and a reduction of AMP-kinase alpha phosphorylation. Glucose 11-18 thymoma viral proto-oncogene 1 Mus musculus 53-56 24728251-7 2014 There was increase in phosphorylation by protein kinase B/Akt serine, improve in insulin signaling and reduce of fasting glucose in mice that swam for 1 hour without overload and mice that swan for 1 hour with overload of 5%. Glucose 121-128 thymoma viral proto-oncogene 1 Mus musculus 58-61 24226527-0 2014 Interplay between the Notch and PI3K/Akt pathways in high glucose-induced podocyte apoptosis. Glucose 58-65 thymoma viral proto-oncogene 1 Mus musculus 37-40 23886627-5 2013 On the other hand, subcellular distribution of the enzyme also depends on the stress and pro-survival signals mediated by the Akt and the p38 pathways and, in non-proliferating cells, on the availability of glucose and lactate. Glucose 207-214 thymoma viral proto-oncogene 1 Mus musculus 126-129 24116164-8 2013 In conclusion, UII increased ROS production by NADPH oxidase, leading to the inhibition of signaling pathways involving glucose transport, such as AKT/PKC/ERK. Glucose 120-127 thymoma viral proto-oncogene 1 Mus musculus 147-150 23909487-1 2013 Insulin inhibits hepatic glucose production through activation of the protein kinase Akt, and any defect in this pathway causes fasting hyperglycaemia in Type 2 diabetes. Glucose 25-32 thymoma viral proto-oncogene 1 Mus musculus 85-88 23935948-5 2013 Akt1 (+/-) mice had a lower body weight than their littermates with less fat mass and normal glucose metabolism. Glucose 93-100 thymoma viral proto-oncogene 1 Mus musculus 0-4 24028189-6 2013 At a therapeutically relevant dose, Akt was activated in the muscle, liver, and adipose at 30 min, correlating with the changes in blood glucose levels. Glucose 137-144 thymoma viral proto-oncogene 1 Mus musculus 36-39 23749168-4 2013 Exogenous PIP3 supplementation (1, 5, or 10 nM) increased the phosphorylation of AKT and PKCzeta/lambda, which in turn upregulated GLUT4 total protein expression as well as its surface expression, glucose uptake, and glucose utilization in cells exposed to HG (25 mM); however, PIP2 had no effect. Glucose 197-204 thymoma viral proto-oncogene 1 Mus musculus 81-84 23749168-4 2013 Exogenous PIP3 supplementation (1, 5, or 10 nM) increased the phosphorylation of AKT and PKCzeta/lambda, which in turn upregulated GLUT4 total protein expression as well as its surface expression, glucose uptake, and glucose utilization in cells exposed to HG (25 mM); however, PIP2 had no effect. Glucose 217-224 thymoma viral proto-oncogene 1 Mus musculus 81-84 23749168-9 2013 This study for the first time demonstrates that PIP3 but not PIP2 plays an important role in GLUT4 upregulation and glucose metabolism mediated by AKT/PKCzeta/lambda phosphorylation. Glucose 116-123 thymoma viral proto-oncogene 1 Mus musculus 147-150 23658008-6 2013 In addition, the phosphorylation levels of AMPK and Akt were markedly reduced by ER stressor, and subsequently, glucose uptake and fatty acid oxidation were also reduced. Glucose 112-119 thymoma viral proto-oncogene 1 Mus musculus 52-55 23500140-5 2013 We found that high glucose increased phospho-Akt, TGF-betaR1 mRNA and protein expression. Glucose 19-26 thymoma viral proto-oncogene 1 Mus musculus 45-48 23724874-2 2013 Because Akt plays a key role in insulin signaling, which leads to glucose transport in skeletal muscle, the predominant tissue in insulin-stimulated glucose disposal, we examined whether insulin-stimulated Akt phosphorylation and (or) glucose transport would be decreased in skeletal muscle of mice lacking functional ATM, compared with muscle from wild-type mice. Glucose 66-73 thymoma viral proto-oncogene 1 Mus musculus 8-11 23531619-10 2013 Elevated SHP-1 expression induced by high glucose levels was directly associated with insulin receptor-beta in vitro and in vivo to prevent insulin-stimulated Akt and ERK phosphorylation. Glucose 42-49 thymoma viral proto-oncogene 1 Mus musculus 159-162 23548624-11 2013 CONCLUSIONS: c-Kit signaling has been shown to affect glucose metabolism via the Akt/GSK-3beta pathway. Glucose 54-61 thymoma viral proto-oncogene 1 Mus musculus 81-84 23124190-0 2013 Alpha-synuclein elicits glucose uptake and utilization in adipocytes through the Gab1/PI3K/Akt transduction pathway. Glucose 24-31 thymoma viral proto-oncogene 1 Mus musculus 91-94 23644114-7 2013 CONCLUSION: Homocysteine lowers the uptake and utilization of glucose by down-regulating PDK1 expression and affecting PI3K/Akt signal pathway to cause disturbance of glucose metabolism. Glucose 62-69 thymoma viral proto-oncogene 1 Mus musculus 124-127 22843013-5 2013 Luteolin and EGCG, but not quercetin, inhibited glucose load-induced insulin receptor substrate-1(IRS-1) tyrosine and Akt phosphorylation in adipose tissue. Glucose 48-55 thymoma viral proto-oncogene 1 Mus musculus 118-121 22843013-8 2013 Quercetin, luteolin, and EGCG inhibited inflammation-evoked IKKbeta activation and IRS-1 serine phosphorylation in adipose tissue, and thereby effectively restored glucose load-stimulated IRS-1 tyrosine and Akt phosphorylation, leading to an increase in insulin-mediated glucose uptake in adipocytes. Glucose 164-171 thymoma viral proto-oncogene 1 Mus musculus 207-210 23204326-0 2013 Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation. Glucose 44-51 thymoma viral proto-oncogene 1 Mus musculus 13-16 22585555-6 2013 Data showed that phosphatidyl inositol 3 kinase, Akt1/2, and the protein kinase A pathways were involved in the increase in glucose uptake induced by polymethoxyflavonoids. Glucose 124-131 thymoma viral proto-oncogene 1 Mus musculus 49-55 23439570-4 2013 Quercetin, but not quercitrin moderately attenuated the effects of TNF-alpha and enhanced the basal and insulin stimulated uptake of glucose in a dose-dependent manner via the activation of the protein kinase B (Akt) and AMP-activated protein kinase (AMPK) pathways. Glucose 133-140 thymoma viral proto-oncogene 1 Mus musculus 212-215 23204326-3 2013 To gain mechanistic insights by which constitutive activation of PI3K or Akt may desensitize insulin-mediated glucose uptake in cardiomyocytes, we examined mice with cardiomyocyte-restricted, constitutive or inducible overexpression of a constitutively activated PI3K or a myristoylated Akt1 (myrAkt1) transgene that also expressed a myc-epitope-tagged glucose transporter type 4 protein (GLUT4). Glucose 110-117 thymoma viral proto-oncogene 1 Mus musculus 73-76 24371503-0 2013 Acute hyperglycemia abolishes ischemic preconditioning by inhibiting Akt phosphorylation: normalizing blood glucose before ischemia restores ischemic preconditioning. Glucose 108-115 thymoma viral proto-oncogene 1 Mus musculus 69-72 23204326-10 2013 Thus, constitutive activation of PI3K and Akt in cardiomyocytes impairs GLUT4-mediated glucose uptake via mechanisms that impair the function of GLUT4 after its plasma-membrane insertion. Glucose 87-94 thymoma viral proto-oncogene 1 Mus musculus 42-45 24371503-13 2013 Normalization of glucose with insulin reversed the inhibition of Akt phosphorylation by HG. Glucose 17-24 thymoma viral proto-oncogene 1 Mus musculus 65-68 22000581-1 2012 Since zinc (Zn) plays an important role in the spermatogenesis and Zn deficiency exacerbated diabetes-induced testicular apoptosis, the present study investigated the effect of Zn deficiency on diabetes-induced testicular Akt-mediated glucose metabolism changes and inflammation. Glucose 235-242 thymoma viral proto-oncogene 1 Mus musculus 222-225 22846604-7 2012 Incubation of isolated skeletal muscles with a dose of a selective Akt inhibitor that eliminated the CR-induced increases in Akt2 phosphorylation prevented CR"s effects on insulin-stimulated glucose uptake, pAS160(Thr642) and pFilamin C(Ser2213) without altering pIR(Tyr1162/1163). Glucose 191-198 thymoma viral proto-oncogene 1 Mus musculus 67-70 22846604-8 2012 These data provide compelling new evidence linking the CR-induced increase in insulin-stimulated Akt2 phosphorylation to CR"s effects on insulin-mediated phosphorylation of Akt substrates and glucose uptake in skeletal muscle. Glucose 192-199 thymoma viral proto-oncogene 1 Mus musculus 97-100 22773877-10 2012 Thus, we have identified an Akt-independent relay from mTORC2 to hepatic lipogenesis that separates the effects of insulin on glucose and lipid metabolism. Glucose 126-133 thymoma viral proto-oncogene 1 Mus musculus 28-31 22000581-4 2012 Western blotting assay revealed that Akt-mediated glucose metabolism signaling was down-regulated in the diabetic testis and was further decreased in diabetic mice with Zn deficiency, reflected by reduced phosphorylation of both Akt and GSK-3beta and increased phosphorylation of glycogen synthase along with a disarrangement of fatty acid metabolism (increased expression of PPAR-alpha and decreased adenosine-monophosphate-activated protein kinase phosphorylation). Glucose 50-57 thymoma viral proto-oncogene 1 Mus musculus 37-40 22000581-4 2012 Western blotting assay revealed that Akt-mediated glucose metabolism signaling was down-regulated in the diabetic testis and was further decreased in diabetic mice with Zn deficiency, reflected by reduced phosphorylation of both Akt and GSK-3beta and increased phosphorylation of glycogen synthase along with a disarrangement of fatty acid metabolism (increased expression of PPAR-alpha and decreased adenosine-monophosphate-activated protein kinase phosphorylation). Glucose 50-57 thymoma viral proto-oncogene 1 Mus musculus 229-232 22548733-9 2012 The phosphorylation of Akt and eNOS and the cGMP concentration were significantly lower in MCECs exposed to high glucose than in those exposed to normal glucose. Glucose 113-120 thymoma viral proto-oncogene 1 Mus musculus 23-26 22548733-9 2012 The phosphorylation of Akt and eNOS and the cGMP concentration were significantly lower in MCECs exposed to high glucose than in those exposed to normal glucose. Glucose 153-160 thymoma viral proto-oncogene 1 Mus musculus 23-26 22528394-9 2012 Taken together, these data demonstrate that NYGGF4 knockdown increases glucose transport in myocytes by activation of the IRS-1/PI3K/AKT insulin pathway. Glucose 71-78 thymoma viral proto-oncogene 1 Mus musculus 133-136 21678423-8 2012 In an in vitro culture system, high glucose and insulin significantly altered TNF-alpha, IL-6, and NO production and arginase activity of macrophages, which was reversed by the treatment with AKT and ERK inhibitors. Glucose 36-43 thymoma viral proto-oncogene 1 Mus musculus 192-195 22217673-9 2012 The phosphorylated AKT levels of skeletal muscle were significantly increased in KK Tbeta(4) group compared with KK control group after glucose stimulation. Glucose 136-143 thymoma viral proto-oncogene 1 Mus musculus 19-22 22800886-12 2012 When cells were stimulated with glucose, increased phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 and serine-threonine kinase (Akt) were observed in MIN6-LRP16. Glucose 32-39 thymoma viral proto-oncogene 1 Mus musculus 147-150 22471389-8 2012 Interestingly, CAF diminished the insulin-stimulated serine phosphorylation of Akt (Ser473) and GSK3beta (Ser9), which may reduce glucose uptake in response to insulin and lipid accumulation. Glucose 130-137 thymoma viral proto-oncogene 1 Mus musculus 79-82 21859425-8 2012 Moreover, the dysregulated transcription of the hepatic glucose metabolic enzymes, including GK (glucokinase), G6Pase (glucose-6-phosphatase) and PEPCK (phosphoenolpyruvate carboxykinase), was recovered by an Akt-dependent pathway. Glucose 56-63 thymoma viral proto-oncogene 1 Mus musculus 209-212 21829168-1 2011 It is well known that insulin can activate both PI3K/Akt pathway, which is responsible for glucose uptake, and MAPK pathway, which is crucial for insulin resistance formation. Glucose 91-98 thymoma viral proto-oncogene 1 Mus musculus 53-56 22284633-6 2012 NYGGF4 acts directly on the IRS1/PI3K/AKT insulin pathway to reduce glucose uptake and transport, impairs mitochondrial function and causes IR, which supports our hypothesis that NYGGF4 may be a useful therapeutic target for obesity-associated IR. Glucose 68-75 thymoma viral proto-oncogene 1 Mus musculus 38-41 22124607-1 2012 AIMS/HYPOTHESIS: Insulin activates insulin receptor protein tyrosine kinase and downstream phosphatidylinositol-3-kinase (PI3K)/Akt signalling in muscle to promote glucose uptake. Glucose 164-171 thymoma viral proto-oncogene 1 Mus musculus 128-131 22139838-8 2012 Furthermore, FAK inhibition also completely blocked short term glucose-induced activation of the Akt/AS160 signaling pathway. Glucose 63-70 thymoma viral proto-oncogene 1 Mus musculus 97-100 22139838-9 2012 In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion. Glucose 46-53 thymoma viral proto-oncogene 1 Mus musculus 360-363 22139838-9 2012 In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion. Glucose 193-200 thymoma viral proto-oncogene 1 Mus musculus 360-363 22139838-9 2012 In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion. Glucose 193-200 thymoma viral proto-oncogene 1 Mus musculus 360-363 22860063-13 2012 The liver appears to be a major site of action, possibly by the suppression of hepatic glucose production via the Akt/FoxO1 axis. Glucose 87-94 thymoma viral proto-oncogene 1 Mus musculus 114-117 21813561-7 2011 We found that apoptosis was increased in both STZ-induced diabetic mice and high-glucose-treated HRVECs, which was due to increased activation of PARP, cleaved caspase3, and reduced expression of Notch1 and p-Akt. Glucose 81-88 thymoma viral proto-oncogene 1 Mus musculus 209-212 21813561-10 2011 Thus, our study demonstrated that Notch1 signaling protects cells from PARP- and NF-kappaB-induced apoptosis under high glucose through the activation of Akt. Glucose 120-127 thymoma viral proto-oncogene 1 Mus musculus 154-157 22172591-6 2012 In contrast, high glucose significantly inhibited tubule formation and eNOS expression through inactivation of Akt, while 5-HT significantly attenuated these actions of high glucose (P<0.01). Glucose 18-25 thymoma viral proto-oncogene 1 Mus musculus 111-114 21854750-0 2011 Epac1-mediated, high glucose-induced renal proximal tubular cells hypertrophy via the Akt/p21 pathway. Glucose 21-28 thymoma viral proto-oncogene 1 Mus musculus 86-89 21613227-6 2011 Overexpression of miR-21 mimicked the action of high glucose, which included a reduction in PTEN expression and a concomitant increase in Akt phosphorylation. Glucose 53-60 thymoma viral proto-oncogene 1 Mus musculus 138-141 21613227-7 2011 In contrast, expression of miR-21 Sponge, to inhibit endogenous miR-21, prevented down-regulation of PTEN and phosphorylation of Akt induced by high glucose. Glucose 149-156 thymoma viral proto-oncogene 1 Mus musculus 129-132 21214427-5 2011 However, a new study has shown that PKBalpha-deficient mice can show enhanced glucose tolerance accompanied by improved beta-cell function and higher insulin sensitivity in adipocytes. Glucose 78-85 thymoma viral proto-oncogene 1 Mus musculus 36-44 21493628-3 2011 This enhanced insulin response overactivates the Akt pathway which increases glucose uptake in the heart, resulting in increased glycogen levels and the formation of polyglucosan inclusions. Glucose 77-84 thymoma viral proto-oncogene 1 Mus musculus 49-52 21501347-4 2011 Insulin enhanced glucose uptake in an additive fashion with increased phosphorylation of Akt and AS160 in FABP3-induced myotubes compared to control cells. Glucose 17-24 thymoma viral proto-oncogene 1 Mus musculus 89-92 21501347-5 2011 This increased glucose uptake in FABP3-induced myotubes with insulin stimulation was found even in the presence of palmitate, in which a significantly higher Akt phosphorylation was detected compared to controls. Glucose 15-22 thymoma viral proto-oncogene 1 Mus musculus 158-161 21214427-6 2011 These findings prompted us to review the relevant literature on the regulation of glucose metabolism by PKB isoforms in liver, skeletal muscle, adipocytes and pancreas. Glucose 82-89 thymoma viral proto-oncogene 1 Mus musculus 104-107 21107520-9 2011 Incubation of isolated islets from carbohydrate-restricted NZO mice or MIN6 cells with palmitate and glucose for 48 h resulted in a dephosphorylation of FOXO1 and thymoma viral proto-oncogene 1 (AKT) without changing the protein levels of both proteins. Glucose 101-108 thymoma viral proto-oncogene 1 Mus musculus 163-193 21107520-9 2011 Incubation of isolated islets from carbohydrate-restricted NZO mice or MIN6 cells with palmitate and glucose for 48 h resulted in a dephosphorylation of FOXO1 and thymoma viral proto-oncogene 1 (AKT) without changing the protein levels of both proteins. Glucose 101-108 thymoma viral proto-oncogene 1 Mus musculus 195-198 20972690-2 2011 We aimed at developing unprecedented metal-based activators of Akt signaling which can potentially find applications as tools for regulating glucose metabolism downstream of Akt or serve as lead structures for developing antidiabetic drugs. Glucose 141-148 thymoma viral proto-oncogene 1 Mus musculus 63-66 21204784-7 2011 Consistent with increased PI3K and Akt activity, the double knock-in mice display enhanced whole body insulin sensitivity and disposal of glucose uptake into muscle tissues. Glucose 138-145 thymoma viral proto-oncogene 1 Mus musculus 35-38 20828573-0 2010 Fas activation in adipocytes impairs insulin-stimulated glucose uptake by reducing Akt. Glucose 56-63 thymoma viral proto-oncogene 1 Mus musculus 83-86 21705841-8 2011 Collectively, Berberine upregulates the activity of Akt possibly via insulin signaling pathway, eventually lowering high blood glucose in alloxan-induced diabetic mice. Glucose 127-134 thymoma viral proto-oncogene 1 Mus musculus 52-55 20153001-5 2011 In addition, phosphatidylinositol-3 kinase and Akt protein expressions were increased when C2C12 myotubes were exposed to IH-901 for up to 3 hours; and these effects including glucose uptake were attenuated by pretreatment with LY294002, a selective phosphatidylinositol-3 kinase inhibitor. Glucose 176-183 thymoma viral proto-oncogene 1 Mus musculus 47-50 21998735-5 2011 Chronic (48 h, 0.4 mM) palmitate treatment blunted glucose/AA-induced activation of CaMKII and ERK and caused a concomitant reduction (~75%) in GSIS/AASIS and autocrine-dependent activation of PKB. Glucose 51-58 thymoma viral proto-oncogene 1 Mus musculus 193-196 21109194-4 2010 These defects were normalized by expression of a constitutively active form of Akt in the islets of betaDKO mice, preserving insulin secretion in response to glucose. Glucose 158-165 thymoma viral proto-oncogene 1 Mus musculus 79-82 21073655-9 2010 Furthermore, high glucose concentrations led to apoptosis of beta-cells by activation of p38MAPK and p53, and dysfunction of beta-cells through phosphatase and tensih homolog (PTEN)-dependent Jun N-terminal kinase (JNK) activation and protein kinase B (AKT/PKB) inhibition, which induced the translocation of forkhead box O1 and pancreatic duodenal homeobox-1, followed by reduced insulin expression and secretion. Glucose 18-25 thymoma viral proto-oncogene 1 Mus musculus 253-260 21073655-10 2010 In conclusion, NOX2-derived ROS could play a critical role in high glucose-induced beta-cell dysfunction through PTEN-dependent JNK activation and AKT inhibition. Glucose 67-74 thymoma viral proto-oncogene 1 Mus musculus 147-150 20828573-4 2010 This decrease in glucose uptake was accompanied by reduced protein expression and diminished phosphorylation of Akt. Glucose 17-24 thymoma viral proto-oncogene 1 Mus musculus 112-115 20164156-4 2010 The coexpression of Akt/PKB in SGLT1-expressing oocytes was followed by an increase in glucose-induced currents. Glucose 87-94 thymoma viral proto-oncogene 1 Mus musculus 20-23 20164156-1 2010 Akt/PKB is known to regulate the facilitative glucose carrier GLUT4. Glucose 46-53 thymoma viral proto-oncogene 1 Mus musculus 0-3 20164156-1 2010 Akt/PKB is known to regulate the facilitative glucose carrier GLUT4. Glucose 46-53 thymoma viral proto-oncogene 1 Mus musculus 4-7 20236253-1 2010 AIM: The protein kinase B (PKB)/Akt is known to stimulate the cellular uptake of glucose and amino acids. Glucose 81-88 thymoma viral proto-oncogene 1 Mus musculus 27-30 20236253-1 2010 AIM: The protein kinase B (PKB)/Akt is known to stimulate the cellular uptake of glucose and amino acids. Glucose 81-88 thymoma viral proto-oncogene 1 Mus musculus 32-35 20164156-4 2010 The coexpression of Akt/PKB in SGLT1-expressing oocytes was followed by an increase in glucose-induced currents. Glucose 87-94 thymoma viral proto-oncogene 1 Mus musculus 24-27 19502418-7 2009 RESULTS: Exposure of MIN6 cells and islets to elevated glucose induced ERK1/2 and PKB phosphorylation, which was further enhanced by palmitate. Glucose 55-62 thymoma viral proto-oncogene 1 Mus musculus 82-85 20107192-9 2010 The phosphoinositide-3-kinase inhibitor LY294002 and dominant-negative Akt inhibited antiapoptotic action of BFT-induced and Pim-1 upregulation in high glucose-challenged cardiomyocytes. Glucose 152-159 thymoma viral proto-oncogene 1 Mus musculus 71-74 19638508-1 2009 A majority of subjects with insulin resistance and hyperinsulinemia can maintain their blood glucose levels normal for the whole life presumably through protein kinase B (Akt)-dependent insulin signaling. Glucose 93-100 thymoma viral proto-oncogene 1 Mus musculus 171-174 20067833-7 2010 Glucose-induced attenuation of IRS-2/Akt-mediated signalling was associated with increased IL-1beta expression. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 37-40 20067833-9 2010 Inhibition of SOCS-1 expression by SOCS-1-specific small interfering RNA restored IRS-2/PI3K-mediated Akt phosphorylation suppressed by high glucose. Glucose 141-148 thymoma viral proto-oncogene 1 Mus musculus 102-105 20067833-11 2010 These results indicated that glucose-induced endogenous IL-1beta expression increased betaTC-6 cells apoptosis by inhibiting, at least in part, IRS-2/Akt-mediated signalling through SOCS-1 upregulation. Glucose 29-36 thymoma viral proto-oncogene 1 Mus musculus 150-153 20003097-2 2010 The role of ATM in insulin signalling has not been firmly resolved for skeletal muscle cells, for which Akt phosphorylation is a pivotal step in stimulation of glucose transport. Glucose 160-167 thymoma viral proto-oncogene 1 Mus musculus 104-107 20043882-4 2010 Hence, in DEDD(-/-) mice, Akt protein levels are diminished in skeletal muscles and adipose tissues, which interferes with the translocation of glucose-transporter 4 (GLUT4) upon insulin stimulation, leading to inefficient incorporation of glucose in these organs. Glucose 144-151 thymoma viral proto-oncogene 1 Mus musculus 26-29 20043882-6 2010 Such multifaceted involvement of DEDD in glucose homeostasis by supporting both insulin secretion (via maintenance of S6K1 activity) and glucose uptake (via stabilizing Akt protein), may suggest an association of DEDD-deficiency with the pathogenesis of type 2 diabetes mellitus. Glucose 41-48 thymoma viral proto-oncogene 1 Mus musculus 169-172 19897600-2 2010 A major effector of the insulin/IGF-I signaling pathway, the serine/threonine protein kinase Akt, mediates cellular processes such as glucose uptake, protein synthesis, cell survival, and growth. Glucose 134-141 thymoma viral proto-oncogene 1 Mus musculus 93-96 19947939-1 2009 The purpose of the present study was to examine the potential effect of IFN-gamma (interferon-gamma) on the cellular content and phosphorylation of PKB (protein kinase B), p70S6k (p70 S6 kinase) and MAPK (mitogen-activated protein kinase), and on the ability of insulin to stimulate the glucose uptake and protein synthesis in mouse C2C12 myotubes. Glucose 287-294 thymoma viral proto-oncogene 1 Mus musculus 148-151 19781620-8 2009 CONCLUSIONS: Saponins and sapogenin activate the PI3K/Akt pathway thus leading to phosphorylation and inactivation of GSK-3 alpha/beta with subsequent stimulation of glycogen synthesis as well as increase of Glut4-dependent glucose transport across the cell membrane. Glucose 224-231 thymoma viral proto-oncogene 1 Mus musculus 54-57 18945941-0 2008 High glucose promotes retinal endothelial cell migration through activation of Src, PI3K/Akt1/eNOS, and ERKs. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 89-93 18461163-6 2008 H(2)O(2) increased the activity of both alpha(1) and alpha(2) AMPK in addition to Akt phosphorylation, and H(2)O(2)-stimulated glucose uptake was not reduced in any of the AMPK transgenic mouse models compared with wild type. Glucose 127-134 thymoma viral proto-oncogene 1 Mus musculus 82-85 19424853-4 2008 In the 7- and 22- month AL groups, glucose administration increased serum insulin levels and also increased phosphorylated (p) levels of the insulin receptor (IR), v-akt murine thymoma viral oncogene homolog (Akt), protein kinase C (PKC) zeta/lambda and the membrane fraction of glucose transporter 4 (mGlut4). Glucose 35-42 thymoma viral proto-oncogene 1 Mus musculus 166-169 19424853-4 2008 In the 7- and 22- month AL groups, glucose administration increased serum insulin levels and also increased phosphorylated (p) levels of the insulin receptor (IR), v-akt murine thymoma viral oncogene homolog (Akt), protein kinase C (PKC) zeta/lambda and the membrane fraction of glucose transporter 4 (mGlut4). Glucose 35-42 thymoma viral proto-oncogene 1 Mus musculus 209-212 18701453-6 2008 High glucose and high insulin augmented activation of Akt, Erk, and p70S6 kinase. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 54-57 18701453-7 2008 Dominant negative Akt, but not dominant negative p70S6 kinase, inhibited GSK3beta phosphorylation induced by high glucose and high insulin, suggesting Akt but not p70S6 kinase was upstream of GSK3beta. Glucose 114-121 thymoma viral proto-oncogene 1 Mus musculus 18-21 19046574-6 2008 Through in vivo and in vitro pharmacological and genetic approaches, we demonstrate the involvement of endothelial NO synthase, AMP-activated protein kinase, and Akt in apelin-stimulated glucose uptake in soleus muscle. Glucose 187-194 thymoma viral proto-oncogene 1 Mus musculus 162-165 18288506-5 2008 The phosphorylation of Akt/PKB enhanced glucose transporter 4 translocation to the plasma membrane; this in turn enhanced the glucose utilization in a dose- and time-dependent manner. Glucose 40-47 thymoma viral proto-oncogene 1 Mus musculus 23-30 18288506-9 2008 On the basis of these results, we proposed that both zinc complexes activated the Akt/PKB-mediated insulin-signaling pathway and improved both glucose utilization and lipid metabolism. Glucose 143-150 thymoma viral proto-oncogene 1 Mus musculus 82-89 18276765-9 2008 In MIN6B1 cells, glucose induced phosphorylation of Akt and AS160, and this was mediated by insulin receptor/IRS-2/phosphatidylinositol 3-kinase independently of changes in cytosolic Ca(2+). Glucose 17-24 thymoma viral proto-oncogene 1 Mus musculus 52-55 18276596-1 2008 The Akt substrate of 160 kDa (AS160) is phosphorylated on Akt substrate (PAS) motifs in response to insulin and contraction in skeletal muscle, regulating glucose uptake. Glucose 155-162 thymoma viral proto-oncogene 1 Mus musculus 4-7 17924084-5 2008 In addition, LPA increased the phosphorylation of AKT-1 with no effects on IRS-1, and LPA-induced glucose uptake was abrogated by pretreatment with the PI 3-kinase inhibitor LY294002. Glucose 98-105 thymoma viral proto-oncogene 1 Mus musculus 50-55 18354169-0 2008 Glucose uptake is limiting in T cell activation and requires CD28-mediated Akt-dependent and independent pathways. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 75-78 18354169-5 2008 To further examine the regulation of glucose uptake, we analyzed CD28 activation of Akt, which appeared necessary for maximal glucose uptake of stimulated cells and which we have shown can promote Glut1 cell surface trafficking. Glucose 37-44 thymoma viral proto-oncogene 1 Mus musculus 84-87 18354169-5 2008 To further examine the regulation of glucose uptake, we analyzed CD28 activation of Akt, which appeared necessary for maximal glucose uptake of stimulated cells and which we have shown can promote Glut1 cell surface trafficking. Glucose 126-133 thymoma viral proto-oncogene 1 Mus musculus 84-87 18354169-6 2008 Consistent with a role for Akt in Glut1 trafficking, transgenic expression of constitutively active myristoylated Akt increased glucose uptake of resting T cells, but did not alter Glut1 protein levels. Glucose 128-135 thymoma viral proto-oncogene 1 Mus musculus 114-117 18354169-8 2008 In support of this model, coexpression of Glut1 and myristoylated Akt transgenes resulted in a synergistic increase in glucose uptake and accumulation of activated T cells in vivo that were largely independent of CD28. Glucose 119-126 thymoma viral proto-oncogene 1 Mus musculus 66-69 18354169-9 2008 Induction of Glut1 protein and Akt regulation of Glut1 trafficking are therefore separable functions of CD28 costimulation that cooperate to promote glucose metabolism for T cell activation and proliferation. Glucose 149-156 thymoma viral proto-oncogene 1 Mus musculus 31-34 17141631-5 2006 These findings demonstrate that Akt1 is required in an isoform-specific manner for orchestrating many of the developmental changes in cellular metabolism that occur at the onset of lactation and establish a role for Akt1 in glucose metabolism. Glucose 224-231 thymoma viral proto-oncogene 1 Mus musculus 32-36 18566543-6 2008 CONCLUSION: Taken together, our results suggest that elevated IRS-2 and altered Akt phosphorylation may be more closely tied to the cause of diabetic kidney disease in db/db mice than mesangial matrix expansion per se, though both may originate from elevated circulatory glucose, and mesangial matrix expansion may independently exacerbate kidney dysfunction. Glucose 271-278 thymoma viral proto-oncogene 1 Mus musculus 80-83 17991718-4 2007 Studies with inhibitors showed that PI3 kinase-Akt-mTOR-p70S6 kinase pathway controlled changes in phosphorylation of eEF2 and eEF2 kinase induced by high glucose or high insulin. Glucose 155-162 thymoma viral proto-oncogene 1 Mus musculus 47-50 18054552-0 2007 Glucose-dependent insulinotropic polypeptide enhances adipocyte development and glucose uptake in part through Akt activation. Glucose 80-87 thymoma viral proto-oncogene 1 Mus musculus 111-114 17609365-7 2007 Further, we show that Akt1(-/-)Akt2(-/-) DN3 cells have decreased glucose uptake and die in response to TCR stimulation in vitro. Glucose 66-73 thymoma viral proto-oncogene 1 Mus musculus 22-26 17538188-8 2007 The stimulatory effect of high glucose on UB branching was blocked in the presence of catalase and inhibitors of NADPH oxidase, mitochondrial electron transport chain complex I, and Akt signaling. Glucose 31-38 thymoma viral proto-oncogene 1 Mus musculus 182-185 17287469-2 2007 In skeletal muscle, activation of AMPK and Akt has been implicated in the regulation of glucose uptake. Glucose 88-95 thymoma viral proto-oncogene 1 Mus musculus 43-46 17267763-5 2007 These results indicate that, if the hepatic abundance of glucokinase is maintained, ingested glucose is normally disposed of even in the absence of acute activation of proximal insulin signaling, such as the activation of Akt, in the liver. Glucose 93-100 thymoma viral proto-oncogene 1 Mus musculus 222-225 17967879-5 2008 Furthermore, insulin-stimulated phosphorylation of the Akt substrate AS160 at Thr642 was reduced in rictor knockout muscle, indicating a defect in insulin signaling to stimulate glucose transport. Glucose 178-185 thymoma viral proto-oncogene 1 Mus musculus 55-58 17875968-3 2007 Furthermore, protein kinase B/Akt inhibition induced by ONOO- or high glucose and apoptosis triggered by high glucose could be abolished by transfection of PTEN-specific small interfering RNA, suggesting that PTEN mediated the Akt inhibition by ONOO-. Glucose 70-77 thymoma viral proto-oncogene 1 Mus musculus 30-33 17875968-3 2007 Furthermore, protein kinase B/Akt inhibition induced by ONOO- or high glucose and apoptosis triggered by high glucose could be abolished by transfection of PTEN-specific small interfering RNA, suggesting that PTEN mediated the Akt inhibition by ONOO-. Glucose 70-77 thymoma viral proto-oncogene 1 Mus musculus 227-230 17875968-3 2007 Furthermore, protein kinase B/Akt inhibition induced by ONOO- or high glucose and apoptosis triggered by high glucose could be abolished by transfection of PTEN-specific small interfering RNA, suggesting that PTEN mediated the Akt inhibition by ONOO-. Glucose 110-117 thymoma viral proto-oncogene 1 Mus musculus 227-230 17141631-5 2006 These findings demonstrate that Akt1 is required in an isoform-specific manner for orchestrating many of the developmental changes in cellular metabolism that occur at the onset of lactation and establish a role for Akt1 in glucose metabolism. Glucose 224-231 thymoma viral proto-oncogene 1 Mus musculus 216-220 16352665-0 2006 Effects of chronic Akt activation on glucose uptake in the heart. Glucose 37-44 thymoma viral proto-oncogene 1 Mus musculus 19-22 16804083-6 2006 Similarly, exposure of mesangial cells to high concentrations of glucose also decreased PTEN expression and its phosphatase activity, resulting in increased Akt activity. Glucose 65-72 thymoma viral proto-oncogene 1 Mus musculus 157-160 16352665-5 2006 Basal glucose uptake was also increased in Akt transgenic mice in vivo (P < 0.005). Glucose 6-13 thymoma viral proto-oncogene 1 Mus musculus 43-46 16352665-11 2006 These data demonstrate that chronic Akt activation increases basal glucose uptake and glycogen deposition while inhibiting the response to insulin. Glucose 67-74 thymoma viral proto-oncogene 1 Mus musculus 36-39 16775839-0 2006 High glucose increase cell cycle regulatory proteins level of mouse embryonic stem cells via PI3-K/Akt and MAPKs signal pathways. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 99-102 16775839-3 2006 Moreover, high glucose level increased the cellular reactive oxygen species (ROS), Akt, and mitogen-activated protein kinases (MAPKs) phosphorylation. Glucose 15-22 thymoma viral proto-oncogene 1 Mus musculus 83-86 16775839-7 2006 High glucose level phosphorylated the RB protein, which was decreased by inhibition of PI3-K and Akt. Glucose 5-12 thymoma viral proto-oncogene 1 Mus musculus 97-100 16775839-8 2006 In conclusion, high glucose level stimulates mouse ES cell proliferation via the PI3-K/Akt and MAPKs pathways. Glucose 20-27 thymoma viral proto-oncogene 1 Mus musculus 87-90 16804076-2 2006 Stimulation of cellular glucose uptake involves phosphatidylinositide-3-kinase (PI-3K)-dependent activation of protein kinase B/Akt. Glucose 24-31 thymoma viral proto-oncogene 1 Mus musculus 128-131 16731820-1 2006 Glucose controls islet beta-cell mass and function at least in part through the phosphatidylinositol 3-kinase (PI3K)/Akt pathway downstream of insulin signaling. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 117-120 16352665-1 2006 Acute activation of the serine-threonine kinase Akt is cardioprotective and increases glucose uptake, at least in part, through enhanced expression of GLUT4 on the sarcolemma. Glucose 86-93 thymoma viral proto-oncogene 1 Mus musculus 48-51 16352665-4 2006 We found that chronic cardiac activation of Akt led to a substantial increase in the rate of basal glucose uptake (P < 0.05) but blunted the response to insulin (1.9 vs. 18.1-fold increase compared with baseline) using NMR in ex vivo perfused heart. Glucose 99-106 thymoma viral proto-oncogene 1 Mus musculus 44-47 16244881-0 2006 Passive stretching produces Akt- and MAPK-dependent augmentations of GLUT4 translocation and glucose uptake in skeletal muscles of mice. Glucose 93-100 thymoma viral proto-oncogene 1 Mus musculus 28-31 16418171-5 2006 This Ser-318 phosphorylation improved insulin-stimulated Akt phosphorylation and glucose uptake in myotubes since transfection with an IRS-1/Glu-318 mutant simulating a permanent phospho-Ser-318 modification increased Akt phosphorylation and glucose uptake. Glucose 81-88 thymoma viral proto-oncogene 1 Mus musculus 218-221 16418171-5 2006 This Ser-318 phosphorylation improved insulin-stimulated Akt phosphorylation and glucose uptake in myotubes since transfection with an IRS-1/Glu-318 mutant simulating a permanent phospho-Ser-318 modification increased Akt phosphorylation and glucose uptake. Glucose 242-249 thymoma viral proto-oncogene 1 Mus musculus 57-60 16418171-5 2006 This Ser-318 phosphorylation improved insulin-stimulated Akt phosphorylation and glucose uptake in myotubes since transfection with an IRS-1/Glu-318 mutant simulating a permanent phospho-Ser-318 modification increased Akt phosphorylation and glucose uptake. Glucose 242-249 thymoma viral proto-oncogene 1 Mus musculus 218-221 16644709-6 2006 At the molecular level, the effects of OFS on endogenous glucose production correlated with changes of hepatic IRS (insulin receptor substrate)-2 and Akt phosphorylation in an Ex-9-dependent manner. Glucose 57-64 thymoma viral proto-oncogene 1 Mus musculus 150-153 16244881-6 2006 Our results suggest that passive stretching produces translocation of GLUT4 mainly from the fraction rich in intracellular membrane to that rich in plasma membrane, and that the glucose uptake could be Akt- and p38 MAPK-dependent, but AMPK-independent manners. Glucose 178-185 thymoma viral proto-oncogene 1 Mus musculus 202-205 16179343-2 2005 We found that Akt and GSK3 are sensitive to glucose, because fasting decreased and glucose administration increased by severalfold the phosphorylation of Akt and GSK3 in the cerebral cortex and hippocampus of non-diabetic mice. Glucose 83-90 thymoma viral proto-oncogene 1 Mus musculus 14-17 16453021-5 2006 Exposure to 20 mM glucose resulted in decreased Akt phosphorylation and enhanced nuclear translocation of forkhead box O3a (FOXO3a). Glucose 18-25 thymoma viral proto-oncogene 1 Mus musculus 48-51 16179343-0 2005 Physiological and pathological changes in glucose regulate brain Akt and glycogen synthase kinase-3. Glucose 42-49 thymoma viral proto-oncogene 1 Mus musculus 65-68 16179343-2 2005 We found that Akt and GSK3 are sensitive to glucose, because fasting decreased and glucose administration increased by severalfold the phosphorylation of Akt and GSK3 in the cerebral cortex and hippocampus of non-diabetic mice. Glucose 44-51 thymoma viral proto-oncogene 1 Mus musculus 14-17 16179343-2 2005 We found that Akt and GSK3 are sensitive to glucose, because fasting decreased and glucose administration increased by severalfold the phosphorylation of Akt and GSK3 in the cerebral cortex and hippocampus of non-diabetic mice. Glucose 83-90 thymoma viral proto-oncogene 1 Mus musculus 154-157 16179343-2 2005 We found that Akt and GSK3 are sensitive to glucose, because fasting decreased and glucose administration increased by severalfold the phosphorylation of Akt and GSK3 in the cerebral cortex and hippocampus of non-diabetic mice. Glucose 44-51 thymoma viral proto-oncogene 1 Mus musculus 154-157 16179343-3 2005 Brain Akt and GSK3 phosphorylation also increased after streptozotocin administration (3 days), which increased blood glucose and depleted blood insulin, indicating regulation by glucose availability even with deficient insulin. Glucose 118-125 thymoma viral proto-oncogene 1 Mus musculus 6-9 16179343-5 2005 Streptozotocin-induced hyperglycemia and increased brain Akt and GSK3 phosphorylation were reversed by lowering blood glucose with insulin administration. Glucose 118-125 thymoma viral proto-oncogene 1 Mus musculus 57-60 16179343-7 2005 Thus, the Akt-GSK3 signaling pathway is regulated in mouse brain in vivo in response to physiological and pathological changes in insulin and glucose. Glucose 142-149 thymoma viral proto-oncogene 1 Mus musculus 10-13 15983249-8 2005 Akt inhibition independently reduced neuronal nitric oxide synthase expression in Schwann cells in low-glucose cultures. Glucose 103-110 thymoma viral proto-oncogene 1 Mus musculus 0-3 15983249-7 2005 Furthermore, Akt phosphorylation in Schwann cells, downregulated by high-glucose conditions, was also restored by rosuvastatin, consistent with the change of neuronal nitric oxide synthase expression. Glucose 73-80 thymoma viral proto-oncogene 1 Mus musculus 13-16 15741651-4 2005 Although the uptake of TG precursors is not stimulated in 3T3-L1 cells with impaired mitochondrial activity, we found a strong stimulation of glucose uptake in AA-treated cells mediated by calcium and phosphatidylinositol 3-kinase/Akt1/glycogen synthase kinase 3beta, a pathway known to trigger the translocation of glucose transporter 4 to the plasma membrane in response to insulin. Glucose 142-149 thymoma viral proto-oncogene 1 Mus musculus 231-235 15546857-4 2005 Additionally, Akt phosphorylation was reduced and responded poorly to glucose stimulation. Glucose 70-77 thymoma viral proto-oncogene 1 Mus musculus 14-17 15743841-1 2005 In adipose tissue, insulin controls glucose and lipid metabolism through the intracellular mediators phosphatidylinositol 3-kinase and serine-threonine kinase AKT. Glucose 36-43 thymoma viral proto-oncogene 1 Mus musculus 159-162 15591229-5 2005 Short-term stimulation induces an additive effect on insulin-induced glucose uptake, and this effect is mediated by phosphorylation of Akt in threonine 308 through PKA/Ca2+-dependent and PI3K-independent pathway, whereas insulin-evoked threonine phosphorylation of Akt is exclusively PI3K-dependent. Glucose 69-76 thymoma viral proto-oncogene 1 Mus musculus 135-138 15591229-5 2005 Short-term stimulation induces an additive effect on insulin-induced glucose uptake, and this effect is mediated by phosphorylation of Akt in threonine 308 through PKA/Ca2+-dependent and PI3K-independent pathway, whereas insulin-evoked threonine phosphorylation of Akt is exclusively PI3K-dependent. Glucose 69-76 thymoma viral proto-oncogene 1 Mus musculus 265-268 15657439-3 2005 Although the PI3K/Akt pathway is a key determinant of the insulin-dependent increase in glucose uptake into muscle and adipose cells, the contribution of this pathway in muscle to whole-body glucose homeostasis is unclear. Glucose 88-95 thymoma viral proto-oncogene 1 Mus musculus 18-21 14998989-3 2004 Activation of both the insulin receptor substrates (IRSs)/Akt and the c-Cbl-associated protein (CAP)/c-Cbl pathways are important in regulating insulin-stimulated glucose transport. Glucose 163-170 thymoma viral proto-oncogene 1 Mus musculus 58-61 15504957-2 2004 Phosphatidylinositol (PI) 3-kinase and Akt play a pivotal role in the stimulation of glucose transport by insulin, but detailed mechanisms are unknown. Glucose 85-92 thymoma viral proto-oncogene 1 Mus musculus 39-42 15504957-3 2004 We and others reported that not only insulin but also platelet-derived growth factor (PDGF) and epidermal growth factor facilitate glucose uptake through GLUT4 translocation by activation of PI 3-kinase and Akt in cultured cells. Glucose 131-138 thymoma viral proto-oncogene 1 Mus musculus 207-210 15161747-3 2004 This increase in glucose transport correlated with enhanced insulin-stimulated activities of phosphatidylinositol 3-kinase, protein kinase B (or Akt), and protein kinase Clambda (PKC-lambda), three key molecules in the insulin-signaling pathway, and was associated with decreased levels of serine-phosphorylated insulin receptor substrate 1 (IRS-1), a molecule implicated in insulin resistance. Glucose 17-24 thymoma viral proto-oncogene 1 Mus musculus 145-148 15384582-2 2004 Cell biological studies indicate that CLD formation in mammary epithelial cells is regulated in part by AKT-dependent increases in glucose uptake. Glucose 131-138 thymoma viral proto-oncogene 1 Mus musculus 104-107 15201165-5 2004 Major effects of AKT activation in the cardiomyocyte are increase in cell size, prevention of apoptosis, and regulation of glucose metabolism. Glucose 123-130 thymoma viral proto-oncogene 1 Mus musculus 17-20 14522993-0 2003 Isoform-specific regulation of insulin-dependent glucose uptake by Akt/protein kinase B. Glucose 49-56 thymoma viral proto-oncogene 1 Mus musculus 67-70 12791994-2 2003 The serine-threonine kinase Akt (PKB) is a principal target of insulin signaling that inhibits hepatic glucose output when glucose is available from food. Glucose 103-110 thymoma viral proto-oncogene 1 Mus musculus 28-31 14633850-1 2003 Akt is critical in insulin-induced metabolism of glucose and lipids. Glucose 49-56 thymoma viral proto-oncogene 1 Mus musculus 0-3 12734207-2 2003 Akt reportedly plays a key role in various cellular actions, including glucose transport, glycogen synthesis, DNA synthesis, anti-apoptotic activity, and cell proliferation. Glucose 71-78 thymoma viral proto-oncogene 1 Mus musculus 0-3 12734207-4 2003 We found that adenovirus-mediated overexpression of myristoylated (myr-) forms of Akt resulted in high glucose transport activity in 3T3-L1 adipocytes, phosphorylated glycogen synthase kinase-3 (GSK3) and enhanced glycogen synthase activity in hepatocytes, and the promotion of DNA synthesis in interleukin-3-dependent 32D cells. Glucose 103-110 thymoma viral proto-oncogene 1 Mus musculus 82-85 12808134-6 2003 Combined depletions of Akt1 plus Akt2 in these cells even more markedly attenuated insulin action on glucose transporter 4 movements, hexose transport activity, and GSK-3 phosphorylation. Glucose 101-108 thymoma viral proto-oncogene 1 Mus musculus 23-27 12595588-12 2003 The specific decrease in Akt phosphorylation in livers of adult offspring suggests that this may be a mechanism for reduced insulin-dependent physiologic events, such as suppression of hepatic glucose production, a defect associated with susceptibility to type II diabetes mellitus. Glucose 193-200 thymoma viral proto-oncogene 1 Mus musculus 25-28 12700340-7 2003 Transduction of the CIT3 mammary epithelial cell line with a recombinant human adenovirus encoding myr-Akt resulted in an increase in glucose transport and lipid biosynthesis, suggesting that Akt plays an important role in regulation of lipid metabolism. Glucose 134-141 thymoma viral proto-oncogene 1 Mus musculus 103-106 12700340-7 2003 Transduction of the CIT3 mammary epithelial cell line with a recombinant human adenovirus encoding myr-Akt resulted in an increase in glucose transport and lipid biosynthesis, suggesting that Akt plays an important role in regulation of lipid metabolism. Glucose 134-141 thymoma viral proto-oncogene 1 Mus musculus 192-195 12181135-3 2002 PKB activity and phosphorylation state were reduced in the presence of 1.2 mM palmitate, which correlates with a decrease in glycolysis (47%), glucose oxidation (84%), and glucose uptake (43%). Glucose 143-150 thymoma viral proto-oncogene 1 Mus musculus 0-3 12217896-0 2002 Glucose promotes pancreatic islet beta-cell survival through a PI 3-kinase/Akt-signaling pathway. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 75-78 12217896-7 2002 Glucose activation of the protein kinase Akt was demonstrated in both insulinoma cells and cultured mouse islets by means of an antibody specific for Ser(473) phospho-Akt and by an in vitro Akt kinase assay. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 41-44 12217896-7 2002 Glucose activation of the protein kinase Akt was demonstrated in both insulinoma cells and cultured mouse islets by means of an antibody specific for Ser(473) phospho-Akt and by an in vitro Akt kinase assay. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 167-170 12217896-7 2002 Glucose activation of the protein kinase Akt was demonstrated in both insulinoma cells and cultured mouse islets by means of an antibody specific for Ser(473) phospho-Akt and by an in vitro Akt kinase assay. Glucose 0-7 thymoma viral proto-oncogene 1 Mus musculus 167-170 12217896-9 2002 Transfection of insulinoma cells with an Akt kinase-dead plasmid (Akt-K179M) resulted in loss of glucose-mediated protection, whereas transfection with a constitutively active Akt enhanced survival in glucose-deprived insulinoma cells. Glucose 97-104 thymoma viral proto-oncogene 1 Mus musculus 41-44 12217896-9 2002 Transfection of insulinoma cells with an Akt kinase-dead plasmid (Akt-K179M) resulted in loss of glucose-mediated protection, whereas transfection with a constitutively active Akt enhanced survival in glucose-deprived insulinoma cells. Glucose 97-104 thymoma viral proto-oncogene 1 Mus musculus 66-69 12217896-9 2002 Transfection of insulinoma cells with an Akt kinase-dead plasmid (Akt-K179M) resulted in loss of glucose-mediated protection, whereas transfection with a constitutively active Akt enhanced survival in glucose-deprived insulinoma cells. Glucose 97-104 thymoma viral proto-oncogene 1 Mus musculus 66-69 12217896-10 2002 The results of these studies defined a novel pathway for glucose-mediated activation of a PI 3-kinase/Akt survival-signaling pathway in islet beta-cells. Glucose 57-64 thymoma viral proto-oncogene 1 Mus musculus 102-105 10954733-5 2000 The serine/threonine kinase Akt/PKB is a major target of insulin-signaling in the regulation of glucose transport via the facilitative glucose transporter (GLUT4) and glycogen synthesis in peripheral tissues. Glucose 96-103 thymoma viral proto-oncogene 1 Mus musculus 28-31 11018758-1 2000 Recent studies suggest that the serine/threonine kinase protein kinase B (PKB or Akt) is involved in the pathway for insulin-stimulated glucose transporter 4 (GLUT4) translocation and glucose uptake. Glucose 136-143 thymoma viral proto-oncogene 1 Mus musculus 74-77 11018758-1 2000 Recent studies suggest that the serine/threonine kinase protein kinase B (PKB or Akt) is involved in the pathway for insulin-stimulated glucose transporter 4 (GLUT4) translocation and glucose uptake. Glucose 136-143 thymoma viral proto-oncogene 1 Mus musculus 81-84 11533044-7 2001 Thus, the characterization of the Akt1 knockout mice and its comparison to the previously reported Akt2 deficiency phenotype reveals the non-redundant functions of Akt1 and Akt2 genes with respect to organismal growth and insulin-regulated glucose metabolism. Glucose 240-247 thymoma viral proto-oncogene 1 Mus musculus 34-38 11533044-7 2001 Thus, the characterization of the Akt1 knockout mice and its comparison to the previously reported Akt2 deficiency phenotype reveals the non-redundant functions of Akt1 and Akt2 genes with respect to organismal growth and insulin-regulated glucose metabolism. Glucose 240-247 thymoma viral proto-oncogene 1 Mus musculus 164-168 10954733-5 2000 The serine/threonine kinase Akt/PKB is a major target of insulin-signaling in the regulation of glucose transport via the facilitative glucose transporter (GLUT4) and glycogen synthesis in peripheral tissues. Glucose 96-103 thymoma viral proto-oncogene 1 Mus musculus 32-35 8940145-0 1996 Expression of a constitutively active Akt Ser/Thr kinase in 3T3-L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation. Glucose 89-96 thymoma viral proto-oncogene 1 Mus musculus 38-41 9648821-5 1998 Both wtPKBalpha and mPKBalpha expression led to a significant increase in the basal uptake of glucose and methyl-aminoisobutyric acid (a substrate for the system A amino acid transporter), at least to a level seen in control cells treated with insulin. Glucose 94-101 thymoma viral proto-oncogene 1 Mus musculus 20-29 8940145-4 1996 The constitutively active Akt induced glucose uptake into adipocytes in the absence of insulin by stimulating translocation of the insulin-responsive glucose transporter 4 to the plasma membrane. Glucose 38-45 thymoma viral proto-oncogene 1 Mus musculus 26-29 8940145-7 1996 These results indicate that Akt can regulate glucose uptake and metabolism. Glucose 45-52 thymoma viral proto-oncogene 1 Mus musculus 28-31 34952629-9 2021 CONCLUSIONS: Our findings indicated improvement of glucose and lipid metabolism by inulin was to activate glucose transport through the translocation of GLUT4 which was mediated by insulin signaling pathway repairment due to decreased expression of RETN and enhanced phosphorylation of IRS and Akt in GDM mice. Glucose 51-58 thymoma viral proto-oncogene 1 Mus musculus 294-297 33799458-9 2021 Taken together, our results demonstrate that phloridzin, an inhibitor of PTP-MEG2, stimulates glucose uptake through the activation of both AMPK and Akt signaling pathways. Glucose 94-101 thymoma viral proto-oncogene 1 Mus musculus 149-152 34678341-9 2022 The high levels of ROS disturbed the PI3K/Akt pathway, causing insulin resistance and increased plasma glucose in the mouse liver. Glucose 103-110 thymoma viral proto-oncogene 1 Mus musculus 42-45 34952629-9 2021 CONCLUSIONS: Our findings indicated improvement of glucose and lipid metabolism by inulin was to activate glucose transport through the translocation of GLUT4 which was mediated by insulin signaling pathway repairment due to decreased expression of RETN and enhanced phosphorylation of IRS and Akt in GDM mice. Glucose 106-113 thymoma viral proto-oncogene 1 Mus musculus 294-297 33809508-5 2021 They also demonstrated exacerbated insulin resistance and glucose intolerance with lower Akt phosphorylation, GLUT4 expression, and renal damage as well as higher reactive oxygen species and interleukin 1 and lower catalase, superoxide dismutase, and glutathione peroxidase levels. Glucose 58-65 thymoma viral proto-oncogene 1 Mus musculus 89-92 33788626-17 2021 : The study reveals that glucose uptake involves GLUT-4 translocation through a mechanism that is likely to involve the upstream effectors of the PI3-K/Akt pathway. Glucose 25-32 thymoma viral proto-oncogene 1 Mus musculus 152-155 34863080-13 2021 Therefore, these findings indicated that puerarin has therapeutic potential for the treatment of PDAC by suppressing glucose uptake and metabolism via Akt/mTOR activity. Glucose 117-124 thymoma viral proto-oncogene 1 Mus musculus 151-154 34331233-8 2021 These data indicate that activation of the glucose-stimulated PI3K/AKT/FoxO1 signaling pathway is significantly blocked in pancreatic beta-cells in HD. Glucose 43-50 thymoma viral proto-oncogene 1 Mus musculus 67-70 33896390-0 2021 Low glucose and serum levels cause an increased inflammatory factor in 3T3-L1 cell through Akt, MAPKs and NF-kB activation. Glucose 4-11 thymoma viral proto-oncogene 1 Mus musculus 91-94 33896390-7 2021 Low glucose and serum levels increased the activation of protein kinase B (also known as Akt), extracellular signal-regulated protein kinase 1/2, p38, c-Jun N-terminal kinase, and nuclear factor (NF) kB at the protein level. Glucose 4-11 thymoma viral proto-oncogene 1 Mus musculus 89-92 33896390-9 2021 These data suggest that low glucose and serum levels increase the levels of inflammatory factors through the activation of Akt, mitogen activated protein kinase, and NF-kappaB signalling pathways. Glucose 28-35 thymoma viral proto-oncogene 1 Mus musculus 123-126 34724097-2 2021 By silencing Akt isoforms individually and in pairs, in Neuro-2a and HT22 cells we observed that, in insulin-sensitive condition, Akt isoforms differentially reduced activation of AS160 and glucose uptake with Akt2 playing the major role. Glucose 190-197 thymoma viral proto-oncogene 1 Mus musculus 13-16 34724097-2 2021 By silencing Akt isoforms individually and in pairs, in Neuro-2a and HT22 cells we observed that, in insulin-sensitive condition, Akt isoforms differentially reduced activation of AS160 and glucose uptake with Akt2 playing the major role. Glucose 190-197 thymoma viral proto-oncogene 1 Mus musculus 130-133 34724097-4 2021 Over-expression of individual isoforms in insulin-sensitive and resistant cells differentially reversed AS160 phosphorylation with concomitant reversal in glucose uptake indicating a compensatory role of Akt isoforms in controlling neuronal insulin signaling. Glucose 155-162 thymoma viral proto-oncogene 1 Mus musculus 204-207 34724097-5 2021 Post-insulin stimulation Akt2 translocated to the membrane the most followed by Akt3 and Akt1, decreasing glucose uptake in the similar order in insulin-sensitive cells. Glucose 106-113 thymoma viral proto-oncogene 1 Mus musculus 89-93 34724097-8 2021 Thus, isoforms play parallel with predominant role by Akt2, and compensatory yet novel role by Akt1 and Akt3 to regulate neuronal insulin signaling, glucose uptake, and insulin-resistance. Glucose 149-156 thymoma viral proto-oncogene 1 Mus musculus 95-99 34331233-7 2021 Consequently, glucose stimulation failed to activate the downstream molecule phosphatidylinositol-3 kinase (PI3K) in 160Q cells, leading to reduced phosphorylation levels of serine-threonine protein kinase AKT and forkhead box protein O1 (FoxO1). Glucose 14-21 thymoma viral proto-oncogene 1 Mus musculus 206-209 34597809-7 2022 Hirsutine exhibited the effects on enhancing glucose consumption and uptake in IR cell models via activating phosphatidylinositol 3-kinase (PI3K)/Akt pathway, which was blocked by PI3K inhibitor LY294002. Glucose 45-52 thymoma viral proto-oncogene 1 Mus musculus 146-149 33794128-10 2021 DISCUSSION AND CONCLUSION: PLP exerts antidiabetic effects via activating the PI3K/AKT signalling pathway, thus improving insulin resistance, glucose, and lipid metabolism in db/db mice. Glucose 142-149 thymoma viral proto-oncogene 1 Mus musculus 83-86 34691353-8 2021 These results validated that Kudzu resistant starch could improve the glucose sensitivity of T2DM mice by modulating IRS-1/PI3K/AKT/Glut4 signaling transduction. Glucose 70-77 thymoma viral proto-oncogene 1 Mus musculus 128-131 34766133-4 2021 The ensuing hyperinsulinemia further activates hepatic aPKC, which first blocks the ability of Akt to suppress gluconeogenic enzyme expression, and later impairs Akt activation, further increasing hepatic glucose production. Glucose 205-212 thymoma viral proto-oncogene 1 Mus musculus 162-165 34314059-6 2021 In addition, BGN regulates glucose metabolism as shown by improved glucose tolerance in mice as well as AMPK/AKT dual pathway-driven enhanced glucose uptake and GLUT4 translocation in L6 myoblast cells. Glucose 142-149 thymoma viral proto-oncogene 1 Mus musculus 109-112 34162834-13 2021 Taken together, PI3K/Akt pathway inhibition mediated high glucose-induced DNMT1 and DNMT3a overexpression, leading to cell autophagy inhibition and apoptosis via TXNIP protein upregulation in Schwann cells of DPN. Glucose 58-65 thymoma viral proto-oncogene 1 Mus musculus 21-24 34427916-13 2022 Metformin treatment significantly recovered the downregulated Akt phosphorylation and VEGF expression in high-glucose conditions. Glucose 110-117 thymoma viral proto-oncogene 1 Mus musculus 62-65 34341463-6 2021 Moreover, enhanced glucose uptake was observed in both preadipocytes and mature adipocytes, which is associated with upregulated phosphorylation of AKT and ERK but reduced p-JNK. Glucose 19-26 thymoma viral proto-oncogene 1 Mus musculus 148-151 34299508-6 2021 In agreement with these results, pretreatment of 3T3-L1 cells with inhibitors of PTP, PI3K, Akt/PKB, and p38 MAPK inhibited glucose uptake induced by application of S. pastorianus extract. Glucose 124-131 thymoma viral proto-oncogene 1 Mus musculus 92-95 34299508-6 2021 In agreement with these results, pretreatment of 3T3-L1 cells with inhibitors of PTP, PI3K, Akt/PKB, and p38 MAPK inhibited glucose uptake induced by application of S. pastorianus extract. Glucose 124-131 thymoma viral proto-oncogene 1 Mus musculus 96-99 35126394-8 2022 We further revealed that IL-25-mediated-IL-17RB signaling rescued the downregulation of Wnt/beta-catenin pathway both in vivo in diabetic mice and in vitro in HUVECs and induced the phosphorylation of AKT and ERK 1/2 in HUVECs under high glucose conditions. Glucose 238-245 thymoma viral proto-oncogene 1 Mus musculus 201-204 35104662-6 2022 Furthermore, we confirmed the inhibited Akt signaling and exacerbated insulin resistance which resulted in high fasting blood glucose in KO mice. Glucose 126-133 thymoma viral proto-oncogene 1 Mus musculus 40-43 35129868-7 2022 These findings indicate that RvE3 likely improves insulin sensitivity, resulting in the upregulation of glucose uptake in adipocytes by activating the PI3K/Akt signaling pathways. Glucose 104-111 thymoma viral proto-oncogene 1 Mus musculus 156-159 35447553-0 2022 Korean naked waxy barley (saechalssal) extract reduces blood glucose in diabetic mice by modulating the PI3K-Akt-GSK3beta pathway. Glucose 61-68 thymoma viral proto-oncogene 1 Mus musculus 109-112 35502441-12 2022 In addition, treatment with 2-O-M alone significantly enhanced the phosphorylation of AKT in muscle tissue, which enhanced glucose uptake in C2C12 myotubes. Glucose 123-130 thymoma viral proto-oncogene 1 Mus musculus 86-89 35275401-7 2022 Furthermore, SSP regulated glucose and lipid metabolism by activating phosphoinositide 3-kinase/Akt signaling pathway. Glucose 27-34 thymoma viral proto-oncogene 1 Mus musculus 96-99 35192202-0 2022 A novel natural PPARgamma agonist, Gypenoside LXXV, ameliorates cognitive deficits by enhancing brain glucose uptake via the activation of Akt/GLUT4 signaling in db/db mice. Glucose 102-109 thymoma viral proto-oncogene 1 Mus musculus 139-142