Glucose induces an acute increase of superoxide dismutase activity in incubated rat pancreatic islets

1999 ◽  
Vol 276 (2) ◽  
pp. C507-C510 ◽  
Author(s):  
Henriette R. Oliveira ◽  
Rui Curi ◽  
Angelo R. Carpinelli
Keyword(s):  
Superoxide Dismutase ◽  
Pancreatic Islets ◽  
High Glucose ◽  
Glucose Concentration ◽  
Pentose Phosphate ◽  
High Glucose Concentration ◽  
Sod Activity ◽  
High Potassium ◽  
Rat Pancreatic Islets ◽  
Short Period

The activity of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSP) in isolated rat pancreatic islets exposed to high glucose concentration for a short period of time (60 min) was determined. High glucose concentration (16.7 mM) did not significantly alter catalase activity. GSP activity was increased by glucose at 5.6 mM, remaining elevated at higher concentrations up to 16.7 mM. However, the activity of SOD increased with glucose concentration, and this increment was closely correlated with the rate of insulin secretion ( r = 0.96). High potassium (30 mM) did not increase SOD activity, suggesting that the increase in intracellular ionic calcium concentration does not stimulate this enzyme activity. α-Ketoisocaproic acid and pyruvate, which are metabolized through the TCA cycle, did not increase SOD activity, indicating that the stimulation of SOD activity might be triggered by a factor produced through glycolysis or the pentose phosphate pathway.

Metabolism and β-cell function of rat pancreatic islets exposed to human interleukin-1β in the presence of a high glucose concentration

1990 ◽  
Vol 26 (3) ◽  
pp. 245-251 ◽  
Author(s):  
Stellan Sandler ◽  
Klaus Bendtzen ◽  
Décio L. Eizirik ◽  
Eva Strandell ◽  
Michael Welsh ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
High Glucose ◽  
Glucose Concentration ◽  
Cell Function ◽  
Interleukin 1Β ◽  
High Glucose Concentration ◽  
Β Cell ◽  
Rat Pancreatic Islets ◽  
Β Cell Function

Effect of CCK-8 on pentose phosphate shunt activity, pyridine nucleotides, and glucokinase of rat islets

1989 ◽  
Vol 256 (1) ◽  
pp. E68-E73 ◽  
Author(s):  
E. J. Verspohl ◽  
I. Breuning ◽  
H. P. Ammon
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Pentose Phosphate ◽  
Dependent Manner ◽  
Hexokinase Activity ◽  
Rat Pancreatic Islets ◽  
Pentose Phosphate Shunt

In rat pancreatic islets the effects of cholecystokinin octapeptide (CCK-8) on pentose phosphate shunt (PPS) activity, glucokinase and hexokinase activity, and NADPH, NADP+, NADH, and NAD+ were studied. By elevating the glucose concentration from 3.0 to 8.3 and 16.7 mM the oxidation of [1-14C]- and [6-14C]glucose and the calculated PPS activity were increased in a concentration-dependent manner; 10 nM CCK-8 enhanced selectively the effect on [1-14C]glucose oxidation thereby increasing the PPS activity but only at an intermediate glucose concentration (8.3 mM). CCK-8 had no effect on glucokinase or hexokinase activity and CCK-8 did not influence glucose utilization. By elevating the glucose concentration, total NADPH and NADH were increased and total NADP+ and NAD+ were decreased. CCK-8 (10 nM) increased selectively NADPH and decreased NADP+ but did not change NADH or NAD+; the effect of CCK-8 on NADPH and NADH was only observed in the presence of an intermediate stimulatory glucose concentration (8.3 mM) but not at either a substimulatory glucose concentration or a maximally stimulatory glucose concentration for insulin release (3.0 or 16.7 mM). The data indicate first that CCK-8 does not act on glucose phosphorylation or glucose utilization and second that CCK-8 increases PPS activity and NADPH levels in rat pancreatic islets. Since the concentrations of glucose necessary for these CCK-8 effects are in the range of 8.3 mM and parallel with those necessary for insulin release as shown in earlier observations, glucose oxidation via pentose phosphate shunt and NADPH are suggested to be related to the CCK-8-modulated insulin release.

High glucose concentration suppresses mesangial laminin B2 gene expression

1991 ◽  
Vol 5 (2-3) ◽  
pp. 118-120 ◽  
Author(s):  
Shigehiro Katayama ◽  
Mari Abe ◽  
Kiyoshi Tanaka ◽  
Akira Omoto ◽  
Kiyohiko Negishi ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Glucose ◽  
Glucose Concentration ◽  
High Glucose Concentration

scholarly journals Sulodexide reduces glucose induced senescence in human retinal endothelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
A. Gericke ◽  
K. Suminska-Jasińska ◽  
A. Bręborowicz
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Glucose Concentration ◽  
Chronic Exposure ◽  
Replicative Senescence ◽  
Population Doubling ◽  
Population Doubling Time ◽  
High Glucose Concentration ◽  
Retinal Endothelial Cells

AbstractChronic exposure of retinal endothelium cells to hyperglycemia is the leading cause of diabetic retinopathy. We evaluated the effect of high glucose concentration on senescence in human retinal endothelial cells (HREC) and modulation of that effect by Sulodexide. Experiments were performed on HREC undergoing in vitro replicative senescence in standard medium or medium supplemented with glucose 20 mmol/L (GLU) or mannitol 20 mnol/L (MAN). Effect of Sulodexide 0.5 LRU/mL (SUL) on the process of HREC senescence was studied. Glucose 20 mmol/L accelerates senescence of HREC: population doubling time (+ 58%, p < 0.001) β-galactosidase activity (+ 60%, p < 0.002) intracellular oxidative stress (+ 65%, p < 0.01), expression of p53 gene (+ 118%, p < 0.001). Senescent HREC had also reduced transendothelial electrical resistance (TEER) (− 30%, p < 0.001). Mannitol 20 mmol/L used in the same scenario as glucose did not induce HREC senescence. In HREC exposed to GLU and SUL, the senescent changes were smaller. HREC, which became senescent in the presence of GLU, demonstrated higher expression of genes regulating the synthesis of Il6 and VEGF-A, which was reflected by increased secretion of these cytokines (IL6 + 125%, p < 0.001 vs control and VEGF-A + 124% p < 0.001 vs control). These effects were smaller in the presence of SUL, and additionally, an increase of TEER in the senescent HREC was observed. Chronic exposure of HREC to high glucose concentration in medium accelerates their senescence, and that process is reduced when the cells are simultaneously exposed to Sulodexide. Additionally, Sulodexide decreases the secretion of IL6 and VEGF-A from senescent HREC and increases their TEER.

scholarly journals The influence of high glucose concentration on the ability of mesenchymal stromal cells to stimulate blood vessel growth

2011 ◽  
Vol 14 (2) ◽  
pp. 32-35 ◽  
Author(s):  
Zhanna Alekseevna Akopyan ◽  
Georgy Vladimirovich Sharonov ◽  
Tatiana Nikolaevna Kochegura ◽  
Natalya Fedorovna Il'yashenko ◽  
Igor Eduardovich Belyanko ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Blood Vessel ◽  
High Glucose ◽  
Glucose Concentration ◽  
Functional Activity ◽  
Human Adipose Tissue ◽  
Diabetic Patients ◽  
High Glucose Concentration ◽  
Vessel Growth ◽  
Negative Effect

Adipose issue is a source of mesenchymal stem cells (MSC) that can be used to stimulate blood vessel growth in ischemic tissues. Various metabolicdisorders including hypeglycemia may have negative effect on therapeutic properties of these cells. Aim. To study the influence of high glucose concentration on functional activity in human adipose tissue. Materials and methods. Flow cytometry and real time PCR were used to study functional activity of cultured MSC from human adipose issue at highglucose concentration. Results. Prolonged (10-12 days) incubation at a high glucose concentration (25 mM) suppressed the ability of MSC to stimulate angiogenesis. Also,glucose modified expression of genes activating and inhibiting angiogenesis but had no effect on MSC proliferation and apoptosis. Conclusion. High glucose concentration suppresses angiogenic activity of MSC in adipose tissue; it may account for incomplete restoration of bloodflow in diabetic patients.

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