PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27363333-0 2016 Perfluorooctane sulfonate-induced insulin resistance is mediated by protein kinase B pathway. perfluorooctane sulfonic acid 0-25 insulin Homo sapiens 34-41 27363333-1 2016 Perfluorooctane sulfonate (PFOS), a persistent organic pollutant, is blamed to be associated with the incidence of insulin resistance in the general human population. perfluorooctane sulfonic acid 0-25 insulin Homo sapiens 115-122 27363333-1 2016 Perfluorooctane sulfonate (PFOS), a persistent organic pollutant, is blamed to be associated with the incidence of insulin resistance in the general human population. perfluorooctane sulfonic acid 27-31 insulin Homo sapiens 115-122 27363333-2 2016 In this study, we found that PFOS inhibited the phosphorylation and activation of protein kinase B (AKT), a key mediator of cellular insulin sensitivity, in human hepatoma HepG2 cells. perfluorooctane sulfonic acid 29-33 insulin Homo sapiens 133-140 27363333-9 2016 Eventually, the inhibition of AKT led to insulin resistance in PFOS-treated cells. perfluorooctane sulfonic acid 63-67 insulin Homo sapiens 41-48 24498028-11 2014 Although the biological effects of PFOS on the elevated levels of fasting serum glucose and insulin levels were observed in both pups and adults of F1, the phenotypes of insulin resistance and glucose intolerance were only evident in the F1 adults. perfluorooctane sulfonic acid 35-39 insulin Homo sapiens 92-99 34969446-0 2022 Exposure to perfluorooctane sulfonate reduced cell viability and insulin release capacity of beta cells. perfluorooctane sulfonic acid 12-37 insulin Homo sapiens 65-72 19114613-8 2009 Increased serum perfluorooctane sulfate (PFOS) concentrations were associated with increased blood insulin (0.14 +/- 0.05, P < 0.01), homeostasis model assessment of insulin resistance (0.14 +/- 0.05, P < 0.01), and beta-cell function (0.15 +/- 0.05, P < 0.01). perfluorooctane sulfonic acid 41-45 insulin Homo sapiens 99-106 34969446-5 2022 PFOS administration also led to lower serum insulin level both in fasting state and after glucose infusion among male mice. perfluorooctane sulfonic acid 0-4 insulin Homo sapiens 44-51 34969446-7 2022 By measuring insulin content in supernatant, 48-hr pretreatment of PFOS (100 mumol/L) decreased the insulin release capacity of beta-TC-6 cells after glucose stimulation. perfluorooctane sulfonic acid 67-71 insulin Homo sapiens 13-20 34969446-7 2022 By measuring insulin content in supernatant, 48-hr pretreatment of PFOS (100 mumol/L) decreased the insulin release capacity of beta-TC-6 cells after glucose stimulation. perfluorooctane sulfonic acid 67-71 insulin Homo sapiens 100-107 34126693-7 2021 Per log-unit increase in branched (br)-PFOS concentration was associated with increased fasting blood glucose (beta = 0.25, 95% CI: 0.18, 0.33), fasting insulin (beta = 2.19, 95% CI: 1.44, 2.93) and HOMA-IR (beta = 0.69, 95% CI: 0.50, 0.89). perfluorooctane sulfonic acid 39-43 insulin Homo sapiens 153-160 32092270-3 2020 Here, by combining in vivo studies with both wild type and gene knockout mice and in vitro studies with mouse islet beta cells (beta-TC-6), we demonstrated clearly that one-hour exposure of perfluorooctane sulfonate (PFOS) stimulated insulin secretion and intracellular calcium level by activating G protein-coupled receptor 40 (GPR40), a vital free fatty acid regulated membrane receptor on islet beta cells. perfluorooctane sulfonic acid 190-215 insulin Homo sapiens 234-241 32305757-0 2020 Perfluorooctane sulfonate acute exposure stimulates insulin secretion via GPR40 pathway. perfluorooctane sulfonic acid 0-25 insulin Homo sapiens 52-59 32305757-3 2020 In this study, the effect of a most concerned PFAS, perfluorooctane sulfonate (PFOS) on insulin secretion in Beta-TC-6 pancreatic cells was studied. perfluorooctane sulfonic acid 52-77 insulin Homo sapiens 88-95 32305757-3 2020 In this study, the effect of a most concerned PFAS, perfluorooctane sulfonate (PFOS) on insulin secretion in Beta-TC-6 pancreatic cells was studied. perfluorooctane sulfonic acid 79-83 insulin Homo sapiens 88-95 32305757-4 2020 The results showed that PFOS acute exposure stimulated insulin secretion and elevated intracellular calcium concentration ([Ca2+]i). perfluorooctane sulfonic acid 24-28 insulin Homo sapiens 55-62 32305757-7 2020 The PFOS-stimulated insulin secretion was inhibited by GW1100, a G Protein-coupled Receptor 40 (GPR40) specific inhibitor, but not affected by GW9662, a specific antagonist to the peroxisome proliferator-activated receptor gamma (PPARgamma). perfluorooctane sulfonic acid 4-8 insulin Homo sapiens 20-27 32305757-8 2020 The observation of RNA silencing further demonstrated that the PFOS-stimulated insulin secretion is, at least partially, via GPR40. perfluorooctane sulfonic acid 63-67 insulin Homo sapiens 79-86 32305757-9 2020 By using specific inhibitors, we found that the GPR40 downstream pathways, phospholipase C (PLC) and L-type Ca2+ channels (LTCC) were involved in PFOS-stimulated [Ca2+]i elevation and insulin secretion. perfluorooctane sulfonic acid 146-150 insulin Homo sapiens 184-191 29324283-5 2018 During the determination process, ECL signal of PFO dots was decreased in a gradual way by the increase of insulin concentration, and the quenching mechanism was also investigated. perfluorooctane sulfonic acid 48-51 insulin Homo sapiens 107-114 32092270-3 2020 Here, by combining in vivo studies with both wild type and gene knockout mice and in vitro studies with mouse islet beta cells (beta-TC-6), we demonstrated clearly that one-hour exposure of perfluorooctane sulfonate (PFOS) stimulated insulin secretion and intracellular calcium level by activating G protein-coupled receptor 40 (GPR40), a vital free fatty acid regulated membrane receptor on islet beta cells. perfluorooctane sulfonic acid 217-221 insulin Homo sapiens 234-241