scholarly journals Glucose uptake and metabolism by red blood cells from fish with different extracellular glucose levels

2012 ◽  
Vol 216 (3) ◽  
pp. 437-446 ◽  
Author(s):  
W. R. Driedzic ◽  
K. A. Clow ◽  
C. E. Short
Keyword(s):  
Red Blood Cells ◽  
Glucose Uptake ◽  
Blood Cells ◽  
Glucose Levels ◽  
Extracellular Glucose ◽  
Uptake And Metabolism

Hypoxia induces apoptosis via two independent pathways in Jurkat cells: differential regulation by glucose

2001 ◽  
Vol 281 (5) ◽  
pp. C1596-C1603 ◽  
Author(s):  
Ricky Malhotra ◽  
Zhiwu Lin ◽  
Claudius Vincenz ◽  
Frank C. Brosius
Keyword(s):  
Cell Death ◽  
Cytochrome C ◽  
Glucose Uptake ◽  
Molecular Mechanisms ◽  
Death Receptor ◽  
Jurkat Cells ◽  
Caspase 9 ◽  
Cytochrome C Release ◽  
Extracellular Glucose ◽  
Uptake And Metabolism

Glucose uptake and metabolism inhibit hypoxia-induced apoptosis in a variety of cell types, but the underlying molecular mechanisms remain poorly understood. In the present study, we explore hypoxia-mediated cell death pathways in Jurkat cells in the presence and absence of extracellular glucose. In the absence of extracellular glucose, hypoxia caused cytochrome c release, caspase 3 and poly(ADP-ribose)polymerase cleavage, and DNA fragmentation; this apoptotic response was blocked by the caspase 9 inhibitor z-LEHD-FMK. The presence of extracellular glucose during hypoxia prevented cytochrome c release and activation of caspase 9 but did not prevent apoptosis in Jurkat cells. In these conditions, overexpression of the caspase 8 inhibitor v-FLIP prevented hypoxia-mediated cell death. Thus hypoxia can stimulate two apoptotic pathways in Jurkat cells, one dependent on cytochrome c release from mitochondria that is prevented by glucose uptake and metabolism, and the other independent of cytochrome c release and resulting from activation of the death receptor pathway, which is accelerated by glucose uptake and metabolism.

Uptake and metabolism of glucose, alanine and lactate by red blood cells of the American eel Anguilla rostrata

1995 ◽  
Vol 198 (4) ◽  
pp. 877-888 ◽  
Author(s):  
J Soengas ◽  
T Moon
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Co2 Production ◽  
Anguilla Rostrata ◽  
Substrate Uptake ◽  
Cell Water ◽  
American Eel ◽  
Simple Diffusion ◽  
Species Specific ◽  
Uptake And Metabolism

The uptake and metabolism of glucose, alanine and lactate were assessed in red blood cells (RBCs) of the American eel Anguilla rostrata. l-Lactate was metabolized at the highest rates as assessed by O2 consumption and CO2 production, followed by glucose and alanine (rates were approximately half of those observed for lactate). A saturable (Km 10.36±0.60 mmol l-1, Jmax 27.42±2.16 µmol 3-OMG l-1 cell water min-1), sodium-independent but cytochalasin-B-sensitive carrier for d-glucose was observed, which was stereospecific and inhibited by other hexoses. These characteristics are in agreement with those reported for the GLUT-1 glucose carrier of human and Japanese eel erythrocytes. These cells also contained a saturable carrier for l-lactate in the concentration range 0­10 mmol l-1 (Km 6.74±0.36 mmol l-1, Jmax 2.29±0.09 mmol lactate l-1 cell water min-1) whereas, at higher concentrations (10­40 mmol l-1), transport occurred by simple diffusion. The carrier was stereospecific, sodium-independent, fully inhibited by alpha-cyano-4-hydroxycinnamate, DIDS and pyruvate, but less sensitive to SITS, IBCLA and pCMBS. We suggest that this carrier is similar to the H+/monocarboxylate carrier found in mammalian RBCs. Despite the fact that l-alanine transport did not saturate, transport was stereospecific because it was inhibited by d-alanine. These experiments do not, therefore, exclude the existence of an alanine carrier in the eel RBC. The rates of substrate uptake exceeded the ability of the RBC to metabolize the substrate (using 1 mmol l-1 extracellular concentration), with uptake rate/metabolic rate ratios being 2 for alanine, 5 for glucose and 151 for lactate. These experiments indicate that uptake does not limit the ability of the American eel RBC to utilize glucose, alanine or lactate, but that the mechanism(s) of substrate uptake is species-specific.

scholarly journals Biochemical Storage Lesions Occurring in Nonirradiated and Irradiated Red Blood Cells: A Brief Review

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
F. Adams ◽  
G. Bellairs ◽  
A. R. Bird ◽  
O. O. Oguntibeju
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Adverse Reactions ◽  
Storage Period ◽  
Osmotic Fragility ◽  
Sodium Potassium ◽  
Glucose Levels ◽  
Neonates And Infants ◽  
The Impact

Red blood cells undergo a series of biochemical fluctuations during 35–42-day storage period at 1°C to 6°C. The sodium/potassium pump is immobilised causing a decrease in intracellular potassium with an increase in cytoplasmic sodium levels, glucose levels decline, and acidosis occurs as a result of low pH levels. The frailty of stored erythrocytes triggers the formation of haemoglobin-containing microparticles and the release of cell-free haemoglobin which may add to transfusion difficulties. Lipid peroxidation, oxidative stress to band 3 structures, and other morphological and structural molecular changes also occur leading to spheroechinocytes and osmotic fragility. These changes that transpire in the red cells during the storage period are referred to as “storage lesions.” It is well documented that gamma irradiation exacerbates storage lesions and the reports of increased potassium levels leading to adverse reactions observed in neonates and infants have been of particular concern. There are, however, remarkably few systematic studies comparing thein vitrostorage lesions of irradiated and nonirradiated red cell concentrates and it has been suggested that the impact of storage lesions on leucocyte reduced red blood cell concentrate (RBCC) is incomplete. The review examines storage lesions in red blood cells and their adverse effects in reference to blood transfusion.

THE UPTAKE OF GLUCOSE INTO CELLS AND THE ROLE OF INSULIN IN GLUCOSE TRANSPORT

1964 ◽  
Vol 42 (6) ◽  
pp. 933-944 ◽  
Author(s):  
Margaret J. Henderson
Keyword(s):  
Cell Membrane ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Glucose Levels ◽  
Insulin Transport ◽  
Rate Limiting Step ◽  
Limiting Step ◽  
Extracellular Glucose ◽  
Rate Limiting

This presentation has been restricted to the role of insulin in glucose transport in muscle cells and deals mainly with experiments using the perfused rat heart. The several possible means for glucose transfer into cells, diffusion, pores, pinocytosis, carriers, and dimerization, have been discussed; and arguments in favor of the carrier theory, namely, specificity, kinetics, inhibition, competition, and counterflow, have been elaborated. Glucose uptake has been considered to consist of three sequential steps: (1) passage of glucose from within the capillary to the cell surface, (2) transport across the cell membrane, and (3) metabolism of glucose within the cell. The first is considered to take place by diffusion and not to be significantly limiting under normal conditions, nor to be influenced by insulin. Transport across the cell membrane is thought to be mainly under the control of insulin and is the major rate-limiting step in glucose uptake when the extracellular glucose levels are in the normal range. Metabolism of glucose within the cell is the major rate-limiting step in glucose uptake when intracellular glucose concentration is so high that its phosphorylation is near saturation.

scholarly journals Glucose Uptake Activity in Murine Red Blood Cells Infected with Babesia microti and Babesia rodhaini

2004 ◽  
Vol 66 (8) ◽  
pp. 945-949 ◽  
Author(s):  
Takashi OHMORI ◽  
Keishi ADACHI ◽  
Yoshimitsu FUKUDA ◽  
Satoshi TAMAHARA ◽  
Naoaki MATSUKI ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Glucose Uptake ◽  
Blood Cells ◽  
Babesia Microti ◽  
Uptake Activity

Abstract T P96: Controlled Brain Glucose Uptake and Metabolism by Ethanol: An Alternative Approach in Improving Stroke Outcome

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Fauzia Akbary ◽  
Changya Peng ◽  
Karam Asmaro ◽  
Ryan Kochanski ◽  
Murali Guthikonda ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Brain Injury ◽  
Lactic Acidosis ◽  
Atpase Activity ◽  
Glucose Uptake ◽  
Brain Damage ◽  
Brain Glucose ◽  
Glut 1 ◽  
Glucose Levels ◽  
Uptake And Metabolism

Introduction: Post-stroke oxygen deficit impairs oxidative phosphorylation of glucose. Surviving brain cells increase anaerobic glycolysis (hyperglycolysis) promoting reactive oxygen species (ROS) synthesis via lactic acidosis and NADPH oxidase (NOX) activation. Hyperglycemia present in 40% of stroke patients with or without diabetes perpetuates hyperglycolysis. Insulin, the only treatment to attenuate hyperglycemia-induced hyperglycolysis, is linked to increased risk of hypoglycemia and mortality. We showed that EtOH reduced ROS-mediated brain damage. Here, we studied whether hyperglycemia/hyperglycolysis-enhanced brain injury are ameliorated by reducing brain glucose uptake and metabolism rather than affecting blood glucose levels. Methods: Sprague-Dawley rats underwent a 2 h right middle cerebral artery occlusion (MCAO). EtOH (1.5 g/kg) or saline was injected IP upon reperfusion, then sacrificed 3 and 24 h later. Energy stores, hyperglycolysis-associated glucose uptake and metabolism, lactic acidosis, and oxidative stress were assessed via ADP/ATP ratio, NAD+/NADH ratio, Na+/K+ ATPase activity, levels of brain and blood glucose, glucose transporter GLUT 1 and 3, lactate, lactate dehydrogenase (LDH), ROS, phosphofructokinase-1 (PFK-1), NOX, and PFK-1 and NOX activity. Results: Ischemic rats showed significant (p<0.01) increase in ADP/ATP and NAD+/NADH ratios, and decrease in Na+/K+ ATPase activity indicating impaired metabolic and neural activity. Increased blood glucose and decreased brain glucose indicate hyperglycemic condition with hyperglycolysis. High levels of GLUT 1 and 3, lactate, LDH , PFK-1, NOX, and ROS support ROS associated hyperglycolysis. EtOH normalized these metabolic parameters to control levels, but only blood glucose remained higher. In sum, EtOH attenuates hyperglycemia-enhance brain injury by reducing glucose uptake and its hyperglycolytic-mediated metabolism under hyperglycemic condition. Conclusion: EtOH administered upon reperfusion is neuroprotective against ROS-mediated brain damage in acute ischemic stroke. It attenuates hyperglycemia-enhanced hyperglycolysis at the level of glucose uptake, utilization, and metabolism rather than reducing serum glucose levels.

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