PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7827801-3 1994 Both epidermal growth factor (0.1-10 ng/ml) and insulin (1 microgram/ml) significantly increased GSH efflux from Hep G2 cells. Glutathione 97-100 insulin Homo sapiens 48-55 7852537-2 1995 There was no activity detected in the absence of reduced glutathione, which indicates that insulin is cleaved in human adipose tissue through reduction of the disulfide bridge between the chains. Glutathione 57-68 insulin Homo sapiens 91-98 34923141-10 2022 Moreover, GFPT2 was within the regulation network of insulin and EGF, and its expression was regulated by reduced glutathione (GSH) and suppressed by the oxidative stress regulator GSK3-beta. Glutathione 114-125 insulin Homo sapiens 53-60 8062515-6 1994 The reduced glutathione concentrations in blood samples from the insulin-dependent and non-insulin-dependent diabetic patient groups were not different from the control group values (P > 0.05). Glutathione 12-23 insulin Homo sapiens 65-72 8062515-6 1994 The reduced glutathione concentrations in blood samples from the insulin-dependent and non-insulin-dependent diabetic patient groups were not different from the control group values (P > 0.05). Glutathione 12-23 insulin Homo sapiens 91-98 8389126-5 1993 The physiological reductant GSH stimulated basal receptor autophosphorylation, but was either without effect (EGF) or inhibited (insulin) activated receptors, and occurred without visible reduction of receptor structure. Glutathione 28-31 insulin Homo sapiens 129-136 1415522-4 1992 In controls and diabetics, insulin infusion with a simultaneous increase in the plasma GSH/GSSG ratio significantly enhanced nonoxidative glucose disposal without affecting oxidative glucose metabolism. Glutathione 87-90 insulin Homo sapiens 27-34 8384616-6 1993 The increases in GSH and GSH + GSSG in CON were associated with decreases in plasma glucose and insulin levels. Glutathione 17-20 insulin Homo sapiens 96-103 8384616-6 1993 The increases in GSH and GSH + GSSG in CON were associated with decreases in plasma glucose and insulin levels. Glutathione 25-28 insulin Homo sapiens 96-103 2112914-0 1990 Reaction of insulin with reduced glutathione. Glutathione 33-44 insulin Homo sapiens 12-19 2112914-1 1990 An aggregate of insulin, molecular weight about 70,000, was formed when it was incubated with GSH. Glutathione 94-97 insulin Homo sapiens 16-23 34923141-10 2022 Moreover, GFPT2 was within the regulation network of insulin and EGF, and its expression was regulated by reduced glutathione (GSH) and suppressed by the oxidative stress regulator GSK3-beta. Glutathione 127-130 insulin Homo sapiens 53-60 3304287-1 1987 Formation of insulin-glutathione mixed disulfides takes place under the conditions of 0.1 M ammonium acetate, neutral pH and without the presence of any enzyme. Glutathione 21-32 insulin Homo sapiens 13-20 34575035-7 2021 A comprehensive analysis of the data allowed proposing a new hypothesis for the etiology of type 2 diabetes that endogenous glutathione deficiency might be a key condition responsible for the impaired folding of proinsulin which triggered an unfolded protein response, ultimately leading to beta-cell apoptosis and disease development. Glutathione 124-135 insulin Homo sapiens 212-222 34439408-4 2021 Importantly, we found that a combined treatment with the cell permeant iron chelator deferiprone and the glutathione precursor N-acetyl cysteine promoted the structural repair of mitochondria and ER, decreased mitochondrial labile iron and ROS levels, and restored glucose-stimulated insulin secretion. Glutathione 105-116 insulin Homo sapiens 284-291 35624890-10 2022 These results suggest GSH supplementation is of considerable benefit to patients above 55 years, not only supporting decreased glycated hemoglobin (HbA1c) and 8-OHdG but also increasing fasting insulin. Glutathione 22-25 insulin Homo sapiens 194-201 2523783-0 1989 Plasma hepatic glutathione S-transferase concentrations after insulin-induced hypoglycaemia in normal subjects and diabetic patients. Glutathione 15-26 insulin Homo sapiens 62-69 34569273-10 2021 Circulating glutathione is oxidized in a manner that significantly cross-correlates with increasing insulin levels and precedes the decrease in cytoplasmic Eh. Glutathione 12-23 insulin Homo sapiens 100-107 3304287-2 1987 Using a SH-free glutathione-agarose column it is demonstrated that the interaction of insulin with glutathione is specific, and increasing the incubation time between these two peptides results in the reduction of insulin disulfide bonds and the production of A and B chains. Glutathione 16-27 insulin Homo sapiens 86-93 3304287-2 1987 Using a SH-free glutathione-agarose column it is demonstrated that the interaction of insulin with glutathione is specific, and increasing the incubation time between these two peptides results in the reduction of insulin disulfide bonds and the production of A and B chains. Glutathione 16-27 insulin Homo sapiens 214-221 3304287-2 1987 Using a SH-free glutathione-agarose column it is demonstrated that the interaction of insulin with glutathione is specific, and increasing the incubation time between these two peptides results in the reduction of insulin disulfide bonds and the production of A and B chains. Glutathione 99-110 insulin Homo sapiens 86-93 3304287-2 1987 Using a SH-free glutathione-agarose column it is demonstrated that the interaction of insulin with glutathione is specific, and increasing the incubation time between these two peptides results in the reduction of insulin disulfide bonds and the production of A and B chains. Glutathione 99-110 insulin Homo sapiens 214-221 718890-2 1978 Diamide, another agent used in studies of insulin action, markedly reduces GSH levels and increases the movement of sugar into the cell. Glutathione 75-78 insulin Homo sapiens 42-49 6429185-2 1984 Insulin-degrading activity in both MN and PMN fractions was activated by reduced glutathione and was inhibited completely by N-ethylmaleimide. Glutathione 81-92 insulin Homo sapiens 0-7 6429185-7 1984 These results demonstrate that diabetes and/or insulin therapy result in increased leukocyte glutathione-dependent insulin-degrading activity. Glutathione 93-104 insulin Homo sapiens 47-54 6429185-7 1984 These results demonstrate that diabetes and/or insulin therapy result in increased leukocyte glutathione-dependent insulin-degrading activity. Glutathione 93-104 insulin Homo sapiens 115-122 7030365-2 1981 In this study the Authors have evaluated the effects of reduced glutathione on insulin-degrading activity of hemolysate. Glutathione 64-75 insulin Homo sapiens 79-86 7030366-2 1981 In this study the Authors have evaluated the effects of reduced glutathione on insulin-degrading activity of erythrocyte membrane fractions. Glutathione 64-75 insulin Homo sapiens 79-86 36318-7 1979 Our data suggest that the insulin-releasing action of leucine depends on the islets" NADPH and reduced glutathione (GSH); in addition, leucine may contribute to insulin secretion by increasing the islet NADPH:NADP ratio and the NADH:NAD ratio. Glutathione 103-114 insulin Homo sapiens 26-33 36318-7 1979 Our data suggest that the insulin-releasing action of leucine depends on the islets" NADPH and reduced glutathione (GSH); in addition, leucine may contribute to insulin secretion by increasing the islet NADPH:NADP ratio and the NADH:NAD ratio. Glutathione 116-119 insulin Homo sapiens 26-33 36318-8 1979 From the data, we assume that the observed increase of NADPH may lead via GSH to an increase in the number of such thiol groups in the beta-cell membrane, which are believed to be related to stimulation of insulin release and, thus, to increase the sensitivity of the beta-cell to stimulation by glucose and/or leucine. Glutathione 74-77 insulin Homo sapiens 206-213 4693-2 1976 Relationship between blood insulin levels and GSH-dependent insulin degrading activity in liver and blood. Glutathione 46-49 insulin Homo sapiens 27-34 4693-2 1976 Relationship between blood insulin levels and GSH-dependent insulin degrading activity in liver and blood. Glutathione 46-49 insulin Homo sapiens 60-67 4693-5 1976 This GSH-dependent insulin degrading activity in plasma was quite similar to that in liver in its nature. Glutathione 5-8 insulin Homo sapiens 19-26 4693-6 1976 In rats, this GSH-dependent insulin degrading activity in the liver and plasma was fluctuated in response to fluctuation in the blood insulin levels, and the GSH-dependent insulin degrading activity in plasma was well correlated with that in the liver. Glutathione 14-17 insulin Homo sapiens 28-35 4693-6 1976 In rats, this GSH-dependent insulin degrading activity in the liver and plasma was fluctuated in response to fluctuation in the blood insulin levels, and the GSH-dependent insulin degrading activity in plasma was well correlated with that in the liver. Glutathione 14-17 insulin Homo sapiens 135-142 4693-6 1976 In rats, this GSH-dependent insulin degrading activity in the liver and plasma was fluctuated in response to fluctuation in the blood insulin levels, and the GSH-dependent insulin degrading activity in plasma was well correlated with that in the liver. Glutathione 14-17 insulin Homo sapiens 135-142 4693-6 1976 In rats, this GSH-dependent insulin degrading activity in the liver and plasma was fluctuated in response to fluctuation in the blood insulin levels, and the GSH-dependent insulin degrading activity in plasma was well correlated with that in the liver. Glutathione 159-162 insulin Homo sapiens 28-35 4693-7 1976 Similarly, in man the GSH-dependent insulin degrading activity in plasma was changed in response to fluctuation in the blood insulin levels. Glutathione 22-25 insulin Homo sapiens 36-43 4693-7 1976 Similarly, in man the GSH-dependent insulin degrading activity in plasma was changed in response to fluctuation in the blood insulin levels. Glutathione 22-25 insulin Homo sapiens 125-132 6322744-4 1983 In contrast to the insulin-degrading activity, which was activated by glutathione in the presence of EDTA, the peptidase activity was not affected by the thiol compound. Glutathione 70-81 insulin Homo sapiens 19-26 6792502-2 1981 The influence of glutathione and N-ethyl maleimide on insulin binding, membrane hexose transport and glycogen synthase activation. Glutathione 17-28 insulin Homo sapiens 54-61 4807800-0 1973 [Preparation and properties of mixed disulfides of insulin with glutathione and thioglycollic acid (author"s transl)]. Glutathione 64-75 insulin Homo sapiens 51-58 1170876-7 1975 Oxidized glutathione was found to be a linear competitive inhibitor vs. both GSH and insulin. Glutathione 9-20 insulin Homo sapiens 85-92 5816924-2 1969 Variation in the plasma insulin level by the administration of glutathione, 2-mercaptopropionylglycine, cysteine and their oxidized type compounds]. Glutathione 63-74 insulin Homo sapiens 24-31 13961136-0 1962 The reduction of serum albumin, insulin and some simple disulphides by glutathione. Glutathione 71-82 insulin Homo sapiens 32-39 13435070-0 1957 [Behavior of serum glutathione in patients of gastric diseases after insulin loading]. Glutathione 19-30 insulin Homo sapiens 69-76 13709288-0 1961 The effect of insulin and tolbutamide on the reduced glutathione concentration in the blood of diabetic and non-diabetic persons. Glutathione 53-64 insulin Homo sapiens 14-21 14810711-0 1951 The blood glutathione level and its response to insulin in diabetic and non-diabetic patients and a case of insulin resistance. Glutathione 10-21 insulin Homo sapiens 48-55 14810711-0 1951 The blood glutathione level and its response to insulin in diabetic and non-diabetic patients and a case of insulin resistance. Glutathione 10-21 insulin Homo sapiens 108-115 33740389-0 2021 The effects of 3 weeks of oral glutathione supplementation on whole body insulin sensitivity in obese males with and without type 2 diabetes: A randomized trial. Glutathione 31-42 insulin Homo sapiens 73-80 33740389-4 2021 Whole body insulin sensitivity increased significantly in the GSH group. Glutathione 62-65 insulin Homo sapiens 11-18 33740389-8 2021 Oral GSH supplementation improves insulin sensitivity in obese subjects with and without T2DM, although it does not alter markers of oxidative stress. Glutathione 5-8 insulin Homo sapiens 34-41 33740389-10 2021 Novelty bullets: Reduced glutathione supplementation increases insulin sensitivity in obese subjects with and without type 2 diabetes H2O2 emission rate from skeletal muscle mitochondria was not affected by glutathione supplementation. Glutathione 27-38 insulin Homo sapiens 65-72 29300728-0 2018 Intensive insulin therapy increases glutathione synthesis rate in surgical ICU patients with stress hyperglycemia. Glutathione 36-47 insulin Homo sapiens 10-17 30072402-11 2018 Enrichment analyses identified elevations in glutathione regulation, insulin signaling, and mitochondrial metabolism in nonresponders pretraining, which was reflected in vivo by higher pretraining PCr recovery rate and insulin sensitivity in these same individuals. Glutathione 45-56 insulin Homo sapiens 219-226 29379070-4 2018 Using cultured 3T3-L1 adipocytes, we established a model of physiologically-derived oxidative stress by inhibiting the cycling of glutathione and thioredoxin, which induced insulin resistance as measured by impaired insulin-stimulated 2-deoxyglucose uptake. Glutathione 130-141 insulin Homo sapiens 173-180 32982400-10 2020 Changes induced by vemurafenib and trametinib in glutathione homeostasis and DNA repair gene expression were also attenuated by insulin. Glutathione 49-60 insulin Homo sapiens 128-135 32305451-4 2020 We propose that maintenance of proper NADH/NAD+ and GSH/GSSG ratios are central to ameliorate insulin resistance, as alterations in these redox couples lead to complex I dysfunction, disruption of SIRT-3 activity, ROS production and impaired beta-oxidation, the latter two being key effectors of insulin resistance. Glutathione 52-55 insulin Homo sapiens 94-101 30577516-5 2018 Insulin sensitivity increased similarly in dysglycemic and normoglycemic men after 12 weeks of exercise, in parallel to similar increases in concentration of plasma glutamine, and decreased concentrations of plasma glutamate, cysteine, taurine, and glutathione. Glutathione 249-260 insulin Homo sapiens 0-7 30577516-6 2018 Change in plasma concentrations of cysteine and glutathione exhibited the strongest correlations to exercise-improved insulin sensitivity, and expression of a cluster of genes essential for oxidative phosphorylation and fatty acid metabolism in both skeletal muscle and adipose tissue, as well as mitochondria-related genes such as mitofilin. Glutathione 48-59 insulin Homo sapiens 118-125 30577516-9 2018 Both acute and long-term exercise may influence transsulphuration and glutathione biosynthesis, linking exercise-improved insulin sensitivity to oxidative stress and mitochondrial function. Glutathione 70-81 insulin Homo sapiens 122-129 29300728-2 2018 We assessed the effects of intensive insulin treatment (IIT) on glutathione synthesis rate and redox balance in cancer patients, who had developed stress hyperglycemia after major surgery. Glutathione 64-75 insulin Homo sapiens 37-44 24947368-5 2014 Amplification of insulin signaling in HepG2 cells by MR was associated with reduced glutathione, where it functions as a cofactor for phosphatase and tensin homolog. Glutathione 84-95 insulin Homo sapiens 17-24 26687633-10 2016 These results indicate that insulin and IGF-1 have the ability to enhance glutathione biosynthesis in neuronal cells via specific up-regulation of GCLM expression. Glutathione 74-85 insulin Homo sapiens 28-35 25299754-7 2016 Cells treated with insulin reverted H(2)O(2)-induced suppression of reduced glutathione levels by blocking oxidized glutathione. Glutathione 76-87 insulin Homo sapiens 19-26 25299754-7 2016 Cells treated with insulin reverted H(2)O(2)-induced suppression of reduced glutathione levels by blocking oxidized glutathione. Glutathione 116-127 insulin Homo sapiens 19-26 28755973-0 2017 l-Cysteine supplementation increases insulin sensitivity mediated by upregulation of GSH and adiponectin in high glucose treated 3T3-L1 adipocytes. Glutathione 85-88 insulin Homo sapiens 37-44 28755973-2 2017 This study examined the hypothesis that LC supplementation positively up regulates the effects of insulin on GSH and glucose metabolism in 3T3-L1 adipocyte model. Glutathione 109-112 insulin Homo sapiens 98-105 28755973-6 2017 Treatment with insulin alone significantly (p < 0.05) reduced ROS levels as well as increased DsbA-L, adiponectin, GCLC, GCLM, GSH, and GLUT-4 protein levels, glucose utilization, and improved total and HMW adiponectin secretion in HG treated adipocytes compared to HG alone. Glutathione 130-133 insulin Homo sapiens 15-22 28755973-8 2017 In addition, LC supplementation along with insulin increased GCLC (21% Vs LC, 14% insulin), GCLM (28% Vs LC, 16% insulin) and GSH (25% Vs LC and insulin) levels compared with the either insulin or LC alone in HG-treated cells. Glutathione 126-129 insulin Homo sapiens 43-50 26493322-5 2015 This review summarizes the literature linking GSH and its related enzymes, GSH peroxidase, glutaredoxins, and glutathione S-transferases, to obesity and its pertinent endpoints (e.g., energy metabolism, inflammation, and insulin resistance). Glutathione 46-49 insulin Homo sapiens 221-228 26389672-3 2015 In this issue, Ferdaoussi, Dai, and colleagues reveal that insulin secretion is amplified by cytosolic isocitrate dehydrogenase-dependent transfer of reducing equivalents, which generates NADPH and reduced glutathione, which in turn activates sentrin/SUMO-specific protease-1 (SENP1). Glutathione 206-217 insulin Homo sapiens 59-66 24849496-3 2015 Moreover, cells treated with insulin increased the H2O2-induced suppression of glutathione levels and exerted an apparent suppressive effect on oxidative products. Glutathione 79-90 insulin Homo sapiens 29-36 22638968-7 2012 It was found that the reaction between GSH and insulin was pH-, O(2)- and temperature-dependent. Glutathione 39-42 insulin Homo sapiens 47-54 24804549-4 2014 Our results demonstrate that, Fe3O4 and its conjugates such as Fe3O4-GSH, Fe3O4-GSH-G4 quenched insulin fluorescence, indicating strong interactions between insulin protein molecule and Fe3O4. Glutathione 69-72 insulin Homo sapiens 96-103 24804549-4 2014 Our results demonstrate that, Fe3O4 and its conjugates such as Fe3O4-GSH, Fe3O4-GSH-G4 quenched insulin fluorescence, indicating strong interactions between insulin protein molecule and Fe3O4. Glutathione 69-72 insulin Homo sapiens 157-164 24678915-1 2014 The glucose stimulation of insulin secretion by pancreatic beta-cells depends on increased production of metabolic coupling factors, among which changes in NADPH and ROS (reactive oxygen species) may alter the glutathione redox state (EGSH) and signal through changes in thiol oxidation. Glutathione 210-221 insulin Homo sapiens 27-34 24456325-5 2014 Moreover, cells treated with insulin increased H2O2-induced suppression of glutathione levels and exerted an apparent suppressive effect on oxidative products. Glutathione 75-86 insulin Homo sapiens 29-36 24740974-1 2014 This work deals with the synthesis of insulin loaded nanoparticles (NPs) composed of thiolated Eudragit L100 (Eul-cys) and reduced glutathione (GSH) as potential nanocarriers for oral delivery of insulin. Glutathione 131-142 insulin Homo sapiens 38-45 24740974-1 2014 This work deals with the synthesis of insulin loaded nanoparticles (NPs) composed of thiolated Eudragit L100 (Eul-cys) and reduced glutathione (GSH) as potential nanocarriers for oral delivery of insulin. Glutathione 144-147 insulin Homo sapiens 38-45 24740974-3 2014 The insulin release from Eul-cys/GSH and Eul-cys NPs in PBS (pH 7.4) shows that GSH can slightly decrease the release rate of insulin. Glutathione 33-36 insulin Homo sapiens 4-11 24561577-0 2014 Rapid reaction of superoxide with insulin-tyrosyl radicals to generate a hydroperoxide with subsequent glutathione addition. Glutathione 103-114 insulin Homo sapiens 34-41 24488754-5 2014 Further reaction of the ruthenium complexes with the oxidized B chain of insulin, in which two cysteine residues are oxidized to cysteine sulfonic acid (Cys-SO3H), and glutathione, which had been oxidized with hydrogen peroxide to convert the cysteine to cysteine sulfonic acid, provided further support for histidine and glutamic acid binding, respectively. Glutathione 168-179 insulin Homo sapiens 73-80 23618488-12 2013 CONCLUSION: This research confirmed that subjects with T2DM after three months supplementation of vitamins demonstrated significantly low level of hypertension, decrease levels of blood glucose, and increase SOD and GSH enzyme activity that can probably reduce insulin resistance by enhanced lowering oxidative stress parameters. Glutathione 216-219 insulin Homo sapiens 261-268 22638968-0 2012 Studies of interaction between insulin and glutathione using electrospray ionization mass spectrometry. Glutathione 43-54 insulin Homo sapiens 31-38 22638968-1 2012 RATIONALE: The interaction of glutathione (GSH) with insulin plays an important role in the degradation or regulation of insulin. Glutathione 30-41 insulin Homo sapiens 53-60 22638968-1 2012 RATIONALE: The interaction of glutathione (GSH) with insulin plays an important role in the degradation or regulation of insulin. Glutathione 30-41 insulin Homo sapiens 121-128 22638968-1 2012 RATIONALE: The interaction of glutathione (GSH) with insulin plays an important role in the degradation or regulation of insulin. Glutathione 43-46 insulin Homo sapiens 53-60 22638968-1 2012 RATIONALE: The interaction of glutathione (GSH) with insulin plays an important role in the degradation or regulation of insulin. Glutathione 43-46 insulin Homo sapiens 121-128 22638968-2 2012 The characterization of the reaction products of GSH and insulin is very important for a proper understanding of the mechanism of insulin regulation of GSH. Glutathione 49-52 insulin Homo sapiens 130-137 22638968-2 2012 The characterization of the reaction products of GSH and insulin is very important for a proper understanding of the mechanism of insulin regulation of GSH. Glutathione 152-155 insulin Homo sapiens 57-64 22638968-2 2012 The characterization of the reaction products of GSH and insulin is very important for a proper understanding of the mechanism of insulin regulation of GSH. Glutathione 152-155 insulin Homo sapiens 130-137 24740974-3 2014 The insulin release from Eul-cys/GSH and Eul-cys NPs in PBS (pH 7.4) shows that GSH can slightly decrease the release rate of insulin. Glutathione 80-83 insulin Homo sapiens 4-11 24740974-3 2014 The insulin release from Eul-cys/GSH and Eul-cys NPs in PBS (pH 7.4) shows that GSH can slightly decrease the release rate of insulin. Glutathione 80-83 insulin Homo sapiens 126-133 23534396-5 2013 Chronic GSH deficiency in old mice and elderly humans was associated with decreased fasted mitochondrial NEFA oxidation and insulin resistance, and these defects were reversed with GSH restoration. Glutathione 8-11 insulin Homo sapiens 124-131 23534396-7 2013 These data suggest that GSH is a novel regulator of mitochondrial NEFA oxidation and insulin resistance in aging. Glutathione 24-27 insulin Homo sapiens 85-92 23534396-8 2013 Chronic GSH deficiency promotes impaired NEFA oxidation and insulin resistance, and GSH restoration reverses these defects. Glutathione 8-11 insulin Homo sapiens 60-67 26201783-8 2013 In addition, MDA levels were higher (p < 0.001) and GSH levels were lower (p = 0.023) in insulin-resistant subjects compared to their insulin-sensitive counterparts. Glutathione 55-58 insulin Homo sapiens 92-99 23386208-7 2013 The release amount of insulin could be regulated by the levels of GSH. Glutathione 66-69 insulin Homo sapiens 22-29 23843789-7 2013 The influence of insulin resistance might be exerted on the level of glutathione-dependent antioxidant enzymes. Glutathione 69-80 insulin Homo sapiens 17-24 22871100-0 2012 Assessment of red blood cell glutathione status in insulin resistance. Glutathione 29-40 insulin Homo sapiens 51-58 22871100-1 2012 The aim of this study was to assess red blood cell glutathione from insulin-sensitive and insulin-resistant individuals before and after an oral glucose dose. Glutathione 51-62 insulin Homo sapiens 68-75 22871100-8 2012 In conclusion, healthy individuals differing in their degree of insulin resistance showed similar red blood cell glutathione concentrations under non-glucose- and glucose-stimulated conditions. Glutathione 113-124 insulin Homo sapiens 64-71 22638968-8 2012 CONCLUSIONS: The results provide insight into the interaction between GSH and insulin. Glutathione 70-73 insulin Homo sapiens 78-85 20205654-1 2010 The in vitro insulin unfolding had been studied using the "equilibrium unfolding" method where protein is unfolded by reducing reagents in the presence of trace amounts of oxidants such as oxidized glutathione. Glutathione 198-209 insulin Homo sapiens 13-20 21848502-5 2012 Results showed that 50 mug/mL of NAC, SDC, GSH, CS, Arg, Azone, SPC, SNP, and 10 mug/mL of SNP had a significant enhancing effect on promoting the transport of insulin across the TR146 cell model. Glutathione 43-46 insulin Homo sapiens 160-167 21848502-7 2012 Therefore, NAC, GSH, CS, SPC, and SNP appear to be safe, effective permeability enhancers that promote the transport of insulin across the TR146 cell-culture model of buccal epithelium and may be potential enhancers for buccal delivery of insulin with both low toxicity and high efficiency. Glutathione 16-19 insulin Homo sapiens 120-127 21871559-0 2011 Activation of promoter activity of the catalytic subunit of gamma-glutamylcysteine ligase (GCL) in brain endothelial cells by insulin requires antioxidant response element 4 and altered glycemic status: implication for GCL expression and GSH synthesis. Glutathione 238-241 insulin Homo sapiens 126-133 21871559-1 2011 Our recent finding that insulin increased the expression of the glutamate-cysteine ligase catalytic subunit (GCLc) with coincident increases in GCL activity and cellular glutathione (GSH) in human brain microvascular endothelial cells (IHECs) suggests a role for insulin in vascular GSH maintenance. Glutathione 170-181 insulin Homo sapiens 24-31 21871559-1 2011 Our recent finding that insulin increased the expression of the glutamate-cysteine ligase catalytic subunit (GCLc) with coincident increases in GCL activity and cellular glutathione (GSH) in human brain microvascular endothelial cells (IHECs) suggests a role for insulin in vascular GSH maintenance. Glutathione 183-186 insulin Homo sapiens 24-31 21871559-1 2011 Our recent finding that insulin increased the expression of the glutamate-cysteine ligase catalytic subunit (GCLc) with coincident increases in GCL activity and cellular glutathione (GSH) in human brain microvascular endothelial cells (IHECs) suggests a role for insulin in vascular GSH maintenance. Glutathione 283-286 insulin Homo sapiens 24-31 21871559-8 2011 The minor effect of pyruvate also ruled out a major role for hypoglycemia (+-insulin)-induced metabolic stress on GSH induction under these conditions. Glutathione 114-117 insulin Homo sapiens 77-84 12466146-5 2003 We depleted hepatic GSH using the GSH synthesis inhibitor l-buthionine-[S,R]-sulfoximine (BSO, 2 mmol/kg body wt ip for 20 days), which reduced insulin sensitivity by 39.1%. Glutathione 20-23 insulin Homo sapiens 144-151 19928053-1 2009 Conditions were found at the analytical level for the solubilization of a recombinant insulin precursor from inclusion bodies in different buffer systems at a wide pH range in the presence of different reducing (dithiothreitol, dithioerythritol) and chaotropic agents (urea, guanidine hydrochloride) and the subsequent renaturation with the use of redox pairs (cysteine-cystine, oxidized glutathione-reduced glutathione, and others). Glutathione 388-399 insulin Homo sapiens 86-93 19928053-1 2009 Conditions were found at the analytical level for the solubilization of a recombinant insulin precursor from inclusion bodies in different buffer systems at a wide pH range in the presence of different reducing (dithiothreitol, dithioerythritol) and chaotropic agents (urea, guanidine hydrochloride) and the subsequent renaturation with the use of redox pairs (cysteine-cystine, oxidized glutathione-reduced glutathione, and others). Glutathione 408-419 insulin Homo sapiens 86-93 19828091-0 2009 Effects on the glutathione pool of the insulin-induced hypoglycaemia test. Glutathione 15-26 insulin Homo sapiens 39-46 19828091-7 2009 The results obtained show that the insulin-induced GH stimulation test produces a decrease in plasma levels of the glutathione pool, that persists at least for 2 hours following the beginning of the test. Glutathione 115-126 insulin Homo sapiens 35-42 17270303-3 2007 Topical iodine protects the dermally applied insulin presumably by inactivation of endogenous sulfhydryls such as glutathione and gamma glutamylcysteine which can reduce the disulfide bonds of the hormone. Glutathione 114-125 insulin Homo sapiens 45-52 15691882-4 2005 Oxidative stress seemed to be the mechanism underlying these effects, since glutathione was able to restore the insulin signaling as well as the insulin-mediated glycogen synthesis. Glutathione 76-87 insulin Homo sapiens 145-152 15691882-6 2005 Again, homocysteine thiolactone (50 microM) prevented insulin-mediated MAPK, GSK-3 and p70 S6K phosphorylation and these effects were blocked by glutathione (250 microM). Glutathione 145-156 insulin Homo sapiens 54-61 15691882-9 2005 Again, these effects seem to be mediated by oxidative stress, since 250 microM glutathione completely abolished the effects of homocysteine thiolactone on insulin-stimulated DNA and protein synthesis. Glutathione 79-90 insulin Homo sapiens 155-162 15169830-1 2004 Decreased glutathione (GSH) levels and gamma-glutamylcysteine ligase (GCL) activity have been observed in diabetic patients, and insulin reportedly increases GSH synthesis via increased GCL catalytic subunit (GCLC) gene expression. Glutathione 158-161 insulin Homo sapiens 129-136 15169830-2 2004 The signaling pathways responsible for mediating insulin effects on GCLC expression and GSH levels, however, are unknown. Glutathione 88-91 insulin Homo sapiens 49-56 15169830-3 2004 The signaling pathways involved in the regulation of GSH synthesis in response to insulin were examined in primary cultured rat hepatocytes. Glutathione 53-56 insulin Homo sapiens 82-89 15169830-4 2004 GSH levels, GCL activity, GCLC protein, and mRNA levels were increased to 140, 160, 600, and 340% of that monitored in untreated cells, respectively, in hepatocytes cultured with 100 nM insulin. Glutathione 0-3 insulin Homo sapiens 186-193 19807652-4 2009 Insulin sensitizers such as biguanides or AMP-activated protein kinase activator, but not glitazones, afforded cytoprotection through preventing (Deltapsi(m) collapse and activation of caspase-9 that was independent of cellular GSH. Glutathione 228-231 insulin Homo sapiens 0-7 19082192-7 2009 These results suggest that GSH concentrations in the RBC may be useful in screening for resistance to C-peptide in vivo. Glutathione 27-30 insulin Homo sapiens 102-111 18926903-0 2008 Insulin stimulation of gamma-glutamylcysteine ligase catalytic subunit expression increases endothelial GSH during oxidative stress: influence of low glucose. Glutathione 104-107 insulin Homo sapiens 0-7 18926903-1 2008 Previously, we demonstrated an important role for insulin in the protection of endothelial cells against hyperglycemic stress through maintaining cellular glutathione (GSH) redox balance. Glutathione 155-166 insulin Homo sapiens 50-57 18926903-1 2008 Previously, we demonstrated an important role for insulin in the protection of endothelial cells against hyperglycemic stress through maintaining cellular glutathione (GSH) redox balance. Glutathione 168-171 insulin Homo sapiens 50-57 18926903-2 2008 The current study focuses on the contribution of insulin to transcriptional control of endothelial cell GSH recovery during acute oxidative challenge and the influence of low glucose. Glutathione 104-107 insulin Homo sapiens 49-56 18926903-3 2008 The results show that insulin induced an approximate 2-fold increase in expression of gamma-glutamylcysteine ligase catalytic subunit (GCLc) mRNA and protein; interestingly, cellular GSH levels were not elevated accordingly. Glutathione 183-186 insulin Homo sapiens 22-29 18926903-4 2008 However, on tert-butylhydroperoxide challenge, insulin-treated cells demonstrated a robust GSH recovery that was attributed to a greater capacity for de novo synthesis via elevated GCLc levels. Glutathione 91-94 insulin Homo sapiens 47-54 18926903-7 2008 Collectively, these results support the functional importance of insulin in Nrf2-dependent transcriptional upregulation of GCLc in GSH recovery during oxidative challenge and suggest a possible role for hypoglycemia in promoting insulin-mediated GCLc upregulation. Glutathione 131-134 insulin Homo sapiens 65-72 18702524-5 2008 In contrast, cysteine and glutathione react more slowly than their selenium analogues with the tyrosyl radical: the reactions of N-acetyl-tyrosyl-amine radicals with cysteine and glutathione are 3 and 5 orders of magnitude slower, respectively, than those with selenocysteine and selenoglutathione, while those of tyrosyl radicals in insulin are 3 and 2 orders of magnitude slower, respectively. Glutathione 26-37 insulin Homo sapiens 334-341 18702524-5 2008 In contrast, cysteine and glutathione react more slowly than their selenium analogues with the tyrosyl radical: the reactions of N-acetyl-tyrosyl-amine radicals with cysteine and glutathione are 3 and 5 orders of magnitude slower, respectively, than those with selenocysteine and selenoglutathione, while those of tyrosyl radicals in insulin are 3 and 2 orders of magnitude slower, respectively. Glutathione 179-190 insulin Homo sapiens 334-341 16631447-2 2006 The objective of this study was to determine the influence of insulin on oxidative stress, defined as a reduced intracellular GSH/GSH disulfide (GSSG) ratio and lipid peroxidation by plasma thiobarbituric acid reactive substances (TBARSs) in patients with type 2 diabetes. Glutathione 126-129 insulin Homo sapiens 62-69 16631447-5 2006 We found a significant elevation in the GSH/GSSG ratio after 2 hours of incubation with insulin in erythrocytes from diabetic patients (11.56+/-1.98 to 15.61+/-2.62, P<.001). Glutathione 40-43 insulin Homo sapiens 88-95 16631447-8 2006 We conclude that insulin in patients with type 2 diabetes mellitus can reduce intracellular oxidative stress through increased GSH/GSSG ratio. Glutathione 127-130 insulin Homo sapiens 17-24 16107611-9 2005 Insulin significantly (P < 0.01) increased oocyte GSH content (6.2 pmol vs. 4.3 pmol) and metformin significantly (P < 0.01) enhanced the action of insulin on GSH content (7.3 pmol vs. 6.2 pmol) and tyrosine kinase activity (1.9 arbitrary units [AU] vs. 1.5 AU) when compared to insulin alone. Glutathione 53-56 insulin Homo sapiens 0-7 16107611-9 2005 Insulin significantly (P < 0.01) increased oocyte GSH content (6.2 pmol vs. 4.3 pmol) and metformin significantly (P < 0.01) enhanced the action of insulin on GSH content (7.3 pmol vs. 6.2 pmol) and tyrosine kinase activity (1.9 arbitrary units [AU] vs. 1.5 AU) when compared to insulin alone. Glutathione 165-168 insulin Homo sapiens 0-7 16107611-9 2005 Insulin significantly (P < 0.01) increased oocyte GSH content (6.2 pmol vs. 4.3 pmol) and metformin significantly (P < 0.01) enhanced the action of insulin on GSH content (7.3 pmol vs. 6.2 pmol) and tyrosine kinase activity (1.9 arbitrary units [AU] vs. 1.5 AU) when compared to insulin alone. Glutathione 165-168 insulin Homo sapiens 154-161 16107611-11 2005 The effects of insulin and metformin were associated with oocyte GSH content and tyrosine kinase activity. Glutathione 65-68 insulin Homo sapiens 15-22 16140208-0 2005 Insulin neuroprotection against oxidative stress in cortical neurons--involvement of uric acid and glutathione antioxidant defenses. Glutathione 99-110 insulin Homo sapiens 0-7 16140208-6 2005 Oxidative stress-induced decreases in intracellular uric acid and GSH/GSSG levels were largely prevented upon treatment with insulin. Glutathione 66-69 insulin Homo sapiens 125-132 16140208-7 2005 Inhibition of phosphatidylinositol-3-kinase (PI-3K) or mitogen-induced extracellular kinase (MEK) reversed the effect of insulin on uric acid and GSH/GSSG, suggesting the activation of insulin-mediated signaling pathways. Glutathione 146-149 insulin Homo sapiens 121-128 16140208-8 2005 Moreover, insulin stimulated glutathione reductase (GRed) and inhibited glutathione peroxidase (GPx) activities under oxidative stress conditions, further supporting that insulin neuroprotection was related to the modulation of the glutathione redox cycle. Glutathione 29-40 insulin Homo sapiens 10-17 16140208-8 2005 Moreover, insulin stimulated glutathione reductase (GRed) and inhibited glutathione peroxidase (GPx) activities under oxidative stress conditions, further supporting that insulin neuroprotection was related to the modulation of the glutathione redox cycle. Glutathione 29-40 insulin Homo sapiens 171-178 15734849-7 2005 Accordingly, 24-h exposure to glutathione significantly improved glucose-stimulated insulin release and decreased nitrotyrosine concentration, with partial recovery of insulin mRNA expression. Glutathione 30-41 insulin Homo sapiens 84-91 15734849-7 2005 Accordingly, 24-h exposure to glutathione significantly improved glucose-stimulated insulin release and decreased nitrotyrosine concentration, with partial recovery of insulin mRNA expression. Glutathione 30-41 insulin Homo sapiens 168-175 15691882-4 2005 Oxidative stress seemed to be the mechanism underlying these effects, since glutathione was able to restore the insulin signaling as well as the insulin-mediated glycogen synthesis. Glutathione 76-87 insulin Homo sapiens 112-119 15169830-7 2004 In conclusion, these data show that insulin signaling pathways involving PI3K/Akt/p70S6K, but not MAPKs, are active in the insulin-mediated regulation of GSH synthesis via increased GCLC expression. Glutathione 154-157 insulin Homo sapiens 36-43 15169830-7 2004 In conclusion, these data show that insulin signaling pathways involving PI3K/Akt/p70S6K, but not MAPKs, are active in the insulin-mediated regulation of GSH synthesis via increased GCLC expression. Glutathione 154-157 insulin Homo sapiens 123-130 12466146-4 2003 Insulin sensitivity was restored to 321.7 +/- 44.7 mg glucose/kg after administration of an NO donor, intraportal SIN-1 (5 mg/kg), which promotes GSH nitrosation, but not after intraportal sodium nitroprusside (20 nmol x kg(-1) x min(-1)), which does not nitrosate GSH. Glutathione 146-149 insulin Homo sapiens 0-7 12466146-4 2003 Insulin sensitivity was restored to 321.7 +/- 44.7 mg glucose/kg after administration of an NO donor, intraportal SIN-1 (5 mg/kg), which promotes GSH nitrosation, but not after intraportal sodium nitroprusside (20 nmol x kg(-1) x min(-1)), which does not nitrosate GSH. Glutathione 265-268 insulin Homo sapiens 0-7 12466146-5 2003 We depleted hepatic GSH using the GSH synthesis inhibitor l-buthionine-[S,R]-sulfoximine (BSO, 2 mmol/kg body wt ip for 20 days), which reduced insulin sensitivity by 39.1%. Glutathione 34-37 insulin Homo sapiens 144-151 12466146-8 2003 These results support our hypothesis that NO and GSH are essential for insulin action. Glutathione 49-52 insulin Homo sapiens 71-78 11896702-0 2002 Reduction of [VO2(ma)2]- and [VO2(ema)2]- by ascorbic acid and glutathione: kinetic studies of pro-drugs for the enhancement of insulin action. Glutathione 63-74 insulin Homo sapiens 128-135 12218186-6 2002 These results demonstrate that glucose and ribose increase islet peroxide accumulation and that the adverse consequences of ribose-induced oxidative stress on insulin mRNA, content, and secretion can be augmented by a glutathione synthesis inhibitor and prevented by increasing islet GPx activity. Glutathione 218-229 insulin Homo sapiens 159-166 11811538-0 2001 Intracellular glutathione deficiency is associated with enhanced nuclear factor-kappaB activation in older non-insulin dependent diabetic patients. Glutathione 14-25 insulin Homo sapiens 111-118 9688536-0 1998 Specific reduction of insulin disulfides by macrophage migration inhibitory factor (MIF) with glutathione and dihydrolipoamide: potential role in cellular redox processes. Glutathione 94-105 insulin Homo sapiens 22-29 11596865-3 2001 Since oxidative stress has been implicated in the development of diabetic complications and GSH plays an important role in protection against oxidative damages, we have studied the in vitro effect of (-)epicatechin and insulin on the reduced glutathione content in normal and type 2 diabetic erythrocytes. Glutathione 242-253 insulin Homo sapiens 219-226 11596865-5 2001 In vitro insulin treatment (10(-9) M) resulted in increase in the GSH content in both normal and type 2 diabetic erythrocytes. Glutathione 66-69 insulin Homo sapiens 9-16 11596865-7 2001 Insulin gave a pronounced dose-responsive effect: maximum increase in GSH content at physiological hormone concentration and a lower increase at higher and lower insulin concentrations. Glutathione 70-73 insulin Homo sapiens 0-7 11488402-7 2001 Last, insulin, which stimulates glycogen synthesis, also increased GSMn(T)/GSH(E) (1.8-fold, P<0.05), as well as GSL(E)/GSH(E) (1.4-fold, P<0.05), in isolated rat soleus muscle. Glutathione 75-78 insulin Homo sapiens 6-13 11488402-7 2001 Last, insulin, which stimulates glycogen synthesis, also increased GSMn(T)/GSH(E) (1.8-fold, P<0.05), as well as GSL(E)/GSH(E) (1.4-fold, P<0.05), in isolated rat soleus muscle. Glutathione 123-126 insulin Homo sapiens 6-13 9711998-9 1998 In conclusion, our data support the hypothesis that abnormal intracellular GSH redox status plays an important role in reducing insulin sensitivity in NIDDM patients. Glutathione 75-78 insulin Homo sapiens 128-135 10491755-4 1999 RESULTS: These conditions resulted in a 50-70% reduction in insulin-stimulated glucose transport activity associated with a decrease in reduced glutathione content from 37.4 +/- 3.1 to 26.4 +/- 4.9 nmol/mg protein, (p < 0.005). Glutathione 144-155 insulin Homo sapiens 60-67 10491755-5 1999 Lipoic acid pretreatment increased insulin-stimulated glucose transport following oxidative stress, reaching 84.8 +/- 4.4% of the control, associated with an increase in reduced glutathione content. Glutathione 178-189 insulin Homo sapiens 35-42 9688536-3 1998 Here we further investigated this function by examining the reduction of insulin disulfides by wild-type human MIF (wtMIF) using various substrates, namely glutathione (GSH), dihydrolipoamide, L-cysteine, beta-mercaptoethanol and dithiothreitol. Glutathione 156-167 insulin Homo sapiens 73-80 9688536-3 1998 Here we further investigated this function by examining the reduction of insulin disulfides by wild-type human MIF (wtMIF) using various substrates, namely glutathione (GSH), dihydrolipoamide, L-cysteine, beta-mercaptoethanol and dithiothreitol. Glutathione 169-172 insulin Homo sapiens 73-80 8927035-6 1995 For example, treatment with two equivalents of glutathione or other thiols the (dipicolinato)peroxovanadate(V) forms (dipicolinato)oxovanadate(V) and vanadate, which are both insulin-mimetic vanadium(V) compounds and can continue to act. Glutathione 47-58 insulin Homo sapiens 175-182