PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25687616-4 2015 Our data demonstrated that these three test 18-carbon PUFAs can inhibit PA-induced interleukin-6 and tumor necrosis factor-alpha messenger RNA (mRNA) expression and IR as evidenced by increases in phosphorylated AKT and the 160-kD AKT substrate, mRNA and plasma membrane protein expression of glucose transporter 4, and glucose uptake. Palmitic Acid 72-74 thymoma viral proto-oncogene 1 Mus musculus 212-215 25687616-4 2015 Our data demonstrated that these three test 18-carbon PUFAs can inhibit PA-induced interleukin-6 and tumor necrosis factor-alpha messenger RNA (mRNA) expression and IR as evidenced by increases in phosphorylated AKT and the 160-kD AKT substrate, mRNA and plasma membrane protein expression of glucose transporter 4, and glucose uptake. Palmitic Acid 72-74 thymoma viral proto-oncogene 1 Mus musculus 231-234 24976766-5 2014 Two EFAs and OA significantly protected PA-induced suppression of insulin signaling, respectively, which was confirmed by the increased levels of Akt phosphorylation and serine/threonine kinases (PKCtheta and JNK) dephosphorylation in the western blot analysis. Palmitic Acid 40-42 thymoma viral proto-oncogene 1 Mus musculus 146-149 25228694-10 2014 Interestingly, we found that palmitic acid stimulated melanoma cell proliferation, changed the cell cycle distribution, and increased phospho-Akt (Ser-473 and Thr-450) and PI3K but not phospho-PTEN (phosphophosphatase and tensin homolog) expressions. Palmitic Acid 29-42 thymoma viral proto-oncogene 1 Mus musculus 142-145 25228694-11 2014 More importantly, the palmitic acid-stimulated proliferation was further enhanced in the Akt-overexpressed melanoma cells and was reduced by LY294002 or knockdown of endogenous Akt or overexpression of Akt mutants. Palmitic Acid 22-35 thymoma viral proto-oncogene 1 Mus musculus 89-92 25228694-11 2014 More importantly, the palmitic acid-stimulated proliferation was further enhanced in the Akt-overexpressed melanoma cells and was reduced by LY294002 or knockdown of endogenous Akt or overexpression of Akt mutants. Palmitic Acid 22-35 thymoma viral proto-oncogene 1 Mus musculus 177-180 25228694-11 2014 More importantly, the palmitic acid-stimulated proliferation was further enhanced in the Akt-overexpressed melanoma cells and was reduced by LY294002 or knockdown of endogenous Akt or overexpression of Akt mutants. Palmitic Acid 22-35 thymoma viral proto-oncogene 1 Mus musculus 177-180 25228694-13 2014 Taken together, we suggest that adipocytes may serve as an exogenous source of palmitic acid that promotes melanoma cell growth by activating Akt. Palmitic Acid 79-92 thymoma viral proto-oncogene 1 Mus musculus 142-145 34643021-2 2021 Results demonstrated that PA reduced insulin sensitivity in SGBS cells with a significant inhibition of Akt phosphorylation, with a higher sensitivity to PA than murine 3T3-L1 adipocytes, GLUT-1 and GLUT-4 glucose transporters and the enzyme hexokinase-II. Palmitic Acid 26-28 thymoma viral proto-oncogene 1 Mus musculus 104-107 24606881-3 2014 PA-pretreated endothelial cells had markedly diminished Akt, eNOS, and ERK activation responses to VEGF, despite normal VEGFR2 phosphorylation. Palmitic Acid 0-2 thymoma viral proto-oncogene 1 Mus musculus 56-59 21158056-5 2009 RESULTS: Chronic PA dose-dependently (1) decreased the availability and increased the apoptosis of MIN6 cells; (2) decreased the phosphorylation of Akt and Bcl-2, but had no significant effects on Akt and Bax. Palmitic Acid 17-19 thymoma viral proto-oncogene 1 Mus musculus 148-151 21158056-5 2009 RESULTS: Chronic PA dose-dependently (1) decreased the availability and increased the apoptosis of MIN6 cells; (2) decreased the phosphorylation of Akt and Bcl-2, but had no significant effects on Akt and Bax. Palmitic Acid 17-19 thymoma viral proto-oncogene 1 Mus musculus 197-200 21158056-6 2009 CONCLUSION: Chronic PA dose-dependently induced apoptosis of MIN6 cells, and this effect was possibly regulated by Akt/Bcl-2. Palmitic Acid 20-22 thymoma viral proto-oncogene 1 Mus musculus 115-118 33039560-7 2021 Consistent with PTEN degradation, exposure of cells to increased concentrations of PA also promoted PTEN-mediated AKT activation and cell proliferation. Palmitic Acid 83-85 thymoma viral proto-oncogene 1 Mus musculus 114-117 34853727-5 2021 Mechanistically, HFD- or PA-initiated lipotoxicity suppressed the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR)/murine double minute 2 homolog (MDM2) signaling cascade to activate p53 and enhance the transcriptional activity of LincRNA-p21. Palmitic Acid 25-27 thymoma viral proto-oncogene 1 Mus musculus 121-124 34295259-5 2021 Next, using an in vitro model of insulin resistance by treating C2C12 cells with palmitic acid (PA), we overexpressed miR-1 and measured p-Akt content and the transcription levels of a protein related to fatty acid oxidation. Palmitic Acid 81-94 thymoma viral proto-oncogene 1 Mus musculus 139-142 34295259-5 2021 Next, using an in vitro model of insulin resistance by treating C2C12 cells with palmitic acid (PA), we overexpressed miR-1 and measured p-Akt content and the transcription levels of a protein related to fatty acid oxidation. Palmitic Acid 96-98 thymoma viral proto-oncogene 1 Mus musculus 139-142 33301311-4 2020 In C2C12 cells, BITC mitigated PA inhibition of glucose uptake and phosphorylation of IRS-1, AKT, and TBC1D1 in response to insulin. Palmitic Acid 31-33 thymoma viral proto-oncogene 1 Mus musculus 93-96 29263047-5 2017 Western blotting was used to detect the activation of the Akt/mTOR signaling pathway and expression of the inflammatory cytokine INF-gamma, in MIN6 cells, following treatments with palmitic acid and palmitic acid+nicotinic acid, or with different concentrations of nicotinic acid and 3-hydroxybutyrate. Palmitic Acid 181-194 thymoma viral proto-oncogene 1 Mus musculus 58-61 32459525-7 2020 In contrast, loss of CPT2 exacerbated PA-induced insulin resistance (acute phospho-Akt; 10 or 100 nM insulin) by as much as ~50-96% compared with WT. Palmitic Acid 38-40 thymoma viral proto-oncogene 1 Mus musculus 83-86 33208251-14 2020 PA-induced reduction in insulin-stimulated phosphorylation of IRS-1, Akt and AS160 and glucose uptake were abolished by co-treatment with HEL. Palmitic Acid 0-2 thymoma viral proto-oncogene 1 Mus musculus 69-72 33208251-15 2020 CONCLUSION: These findings give new insights about the effect of HEL ameliorating PA- impaired IRS-1/Akt/AS160 pathway and glucose uptake in adipocytes. Palmitic Acid 82-84 thymoma viral proto-oncogene 1 Mus musculus 101-104 29374854-12 2018 In addition, liraglutide can reverse PA-decreased insulin-stimulated cell-surface GLUT4 levels, Akt, PI3K(p85alpha), and AS160 phosphorylation. Palmitic Acid 37-39 thymoma viral proto-oncogene 1 Mus musculus 96-99 29263047-5 2017 Western blotting was used to detect the activation of the Akt/mTOR signaling pathway and expression of the inflammatory cytokine INF-gamma, in MIN6 cells, following treatments with palmitic acid and palmitic acid+nicotinic acid, or with different concentrations of nicotinic acid and 3-hydroxybutyrate. Palmitic Acid 199-212 thymoma viral proto-oncogene 1 Mus musculus 58-61 29263047-7 2017 Palmitic acid enhanced the phosphorylation of Akt and p70S6K and elevated the expression of IFN-gamma. Palmitic Acid 0-13 thymoma viral proto-oncogene 1 Mus musculus 46-49 29263047-8 2017 Co-treatment with nicotinic acid, which is an agonist of GPR109A, inhibited the palmitic acid-induced phosphorylation of Akt, mTOR, and p70S6K, as well as the expression of IFN-gamma. Palmitic Acid 80-93 thymoma viral proto-oncogene 1 Mus musculus 121-124 27117849-8 2016 Furthermore, palmitic acid (C16:0) disturbed the insulin-induced phosphorylation of Akt, while MCFAs, including lauric (C12:0), capric (C10:0), and caprylic acid (C12:0), did not. Palmitic Acid 13-26 thymoma viral proto-oncogene 1 Mus musculus 84-87 28265821-9 2017 Moreover, DN-AMPKalpha2 lentivirus and AMPKalpha2 siRNA were transfected into PA-treated L6 myotubes, and the decrease in SREBP-1c expression caused by insulin was blocked by AMPK inhibition independent of the phosphatidylinositol-4,5-biphosphate-3-kinase (PI3K)/AKT pathway. Palmitic Acid 78-80 thymoma viral proto-oncogene 1 Mus musculus 263-266 27928692-0 2017 Palmitic acid triggers cell apoptosis in RGC-5 retinal ganglion cells through the Akt/FoxO1 signaling pathway. Palmitic Acid 0-13 thymoma viral proto-oncogene 1 Mus musculus 82-85 27928692-9 2017 Moreover, PA significantly decreased the level of phospho-Akt and phospho-FoxO1 in cells. Palmitic Acid 10-12 thymoma viral proto-oncogene 1 Mus musculus 58-61 27928692-10 2017 Finally, shRNA knockdown and plasmid overexpression studies displayed that downregulation of Akt protein or upregulation of FoxO1 protein augmented cell death, while knockdown of FoxO1 or overexpression of Akt1 abolished PA-induced cell death. Palmitic Acid 221-223 thymoma viral proto-oncogene 1 Mus musculus 206-210 27928692-11 2017 Collectively, our results indicated that PA-induced cell death is mediated through modulation of Akt/FoxO1 pathway activity. Palmitic Acid 41-43 thymoma viral proto-oncogene 1 Mus musculus 97-100 28123432-6 2016 Western blot analysis revealed that NGF induced the phosphorylation of Akt/FoxO1 and ERK1/2 and reversed the PA-evoked reduction in the levels of these proteins. Palmitic Acid 109-111 thymoma viral proto-oncogene 1 Mus musculus 71-74 26848161-5 2016 Moreover, IKKalpha null macrophages treated with lipotoxic palmitic acid exhibited early exhaustion of Akt signaling compared with wild-type cells. Palmitic Acid 59-72 thymoma viral proto-oncogene 1 Mus musculus 103-106 26436985-4 2016 Moreover, the addition of long-chain PUFAs decreased PA-induced insulin resistance as evidenced by increases in phosphorylated AKT and glucose uptake. Palmitic Acid 53-55 thymoma viral proto-oncogene 1 Mus musculus 127-130 26643367-4 2015 Here, we report that EPO administration promoted phosphatidylinositol 3-kinase (PI3K)/AKT pathway activation in palmitic acid (PA)-treated HepG2 cells and in the liver of high-fat diet (HFD)-fed mice, whereas adenovirus-mediated silencing of the erythropoietin receptor (EPOR) blocked EPO-induced AKT signalling in HepG2 cells. Palmitic Acid 112-125 thymoma viral proto-oncogene 1 Mus musculus 297-300 26643367-4 2015 Here, we report that EPO administration promoted phosphatidylinositol 3-kinase (PI3K)/AKT pathway activation in palmitic acid (PA)-treated HepG2 cells and in the liver of high-fat diet (HFD)-fed mice, whereas adenovirus-mediated silencing of the erythropoietin receptor (EPOR) blocked EPO-induced AKT signalling in HepG2 cells. Palmitic Acid 127-129 thymoma viral proto-oncogene 1 Mus musculus 297-300