scholarly journals Factors Influencing Glucose Flux and the Effect of Insulin in Cultured Human Cells

1967 ◽  
Vol 50 (6) ◽  
pp. 1663-1680 ◽  
Author(s):  
Robert J. Hay ◽  
John Paul
Keyword(s):  
Glucose Uptake ◽  
Osmotic Pressure ◽  
Mercuric Chloride ◽  
Mode Of Action ◽  
Carrier System ◽  
Factors Influencing ◽  
Glucose Flux ◽  
Saturation Kinetics ◽  
Cultured Human Cells ◽  
Glucose Carrier

Uptake of glucose-3H into cultured HLM cells was measured. Equilibration of intracellular and extracellular pools occurred after 25 min. Glucose influx was determined subsequently by measuring the glucose-3H entering in precisely 1 min. Although saturation kinetics were demonstrated these were not of the simple Michaelis-Menten type. The Km of the glucose carrier system is probably about 60 mM glucose. Galactose did not compete with glucose. Insulin stimulated glucose flux without increasing the value of Vmax. The stimulation was fully demonstrable after 10 min, could be elicited at concentrations of 10-4 units/ml, and was absent 2–4 hr after removal. Increasing pH had little or no effect in stimulating glucose flux. Increasing osmotic pressure caused a marked increase and reduced the effect of insulin. Glucose influx was unaffected by anoxia. Glucose influx was increased and the effect of insulin abolished in the absence of K+. Glucose influx was increased by mercuric chloride, iodoacetate, and fluoride which abolished the effect of insulin. Dinitrophenol decreased the rate of glucose uptake but did not alter the effect of insulin. Phlorizin reduced the rate of glucose uptake and abolished the effect of insulin. ATP and AMP enhanced the rate of glucose uptake. These findings are discussed in relation to the mode of action of insulin.

Fiber type-specific determinants of V maxfor insulin-stimulated muscle glucose uptake in vivo

2003 ◽  
Vol 284 (3) ◽  
pp. E541-E548 ◽  
Author(s):  
Hilary Ann Petersen ◽  
Patrick T. Fueger ◽  
Deanna P. Bracy ◽  
David H. Wasserman ◽  
Amy E. Halseth
Keyword(s):  
Glucose Uptake ◽  
Fiber Type ◽  
Type I ◽  
Fiber Types ◽  
Maximal Velocity ◽  
Glucose Flux ◽  
Steady State Levels ◽  
Type I Fibers ◽  
Relationship Of

The aim of this study was to determine barriers limiting muscle glucose uptake (MGU) during increased glucose flux created by raising blood glucose in the presence of fixed insulin. The determinants of the maximal velocity ( V max) of MGU in muscles of different fiber types were defined. Conscious rats were studied during a 4 mU · kg−1 · min−1insulin clamp with plasma glucose at 2.5, 5.5, and 8.5 mM. [U-14C]mannitol and 3- O-methyl-[3H]glucose ([3H]MG) were infused to steady-state levels ( t = −180 to 0 min). These isotope infusions were continued from 0 to 40 min with the addition of a 2-deoxy-[3H]glucose ([3H]DG) infusion. Muscles were excised at t = 40 min. Glucose metabolic index (Rg) was calculated from muscle-phosphorylated [3H]DG. [U-14C]mannitol was used to determine extracellular (EC) H2O. Glucose at the outer ([G]om) and inner ([G]im) sarcolemmal surfaces was determined by the ratio of [3H]MG in intracellular to EC H2O and muscle glucose. Rg was comparable at the two higher glucose concentrations, suggesting that rates of uptake near V max were reached. In summary, by defining the relationship of arterial glucose to [G]om and [G]im in the presence of fixed hyperinsulinemia, it is concluded that 1) V max for MGU is limited by extracellular and intracellular barriers in type I fibers, as the sarcolemma is freely permeable to glucose; 2) V max is limited in muscles with predominantly type IIb fibers by extracellular resistance and transport resistance; and 3) limits to Rg are determined by resistance at multiple steps and are better defined by distributed control rather than by a single rate-limiting step.

Use of 3-O-methyI-D-glucose and phloretin to estimate the intracellular water space of mouse peritoneal macrophage monolayers

1982 ◽  
Vol 60 (1) ◽  
pp. 76-79
Author(s):  
Douglas B. Lowrie
Keyword(s):  
Glucose Uptake ◽  
Peritoneal Macrophage ◽  
Intracellular Water ◽  
Mouse Peritoneal Macrophage ◽  
Facilitated Diffusion ◽  
Water Space ◽  
Glucose Carrier

Macrophages took up 3-O-methyl-D-glucose rapidly by facilitated diffusion using the glucose carrier and slowly by carrier-independent diffusion. Phloretin inhibited carrier-dependent but not carrier-independent diffusion. Estimates of intracellular water space based on 3-O-methyl-D-glucose uptake varied between 0.7 and 6.9 μL∙106 cells−1 for 2-week-old monolayers.

scholarly journals The disposition of carbohydrate between glycogenesis, lipogenesis and oxidation in liver during the starved-to-fed transition

1988 ◽  
Vol 252 (2) ◽  
pp. 325-330 ◽  
Author(s):  
M J Holness ◽  
P A MacLennan ◽  
T N Palmer ◽  
M C Sugden
Keyword(s):  
Glucose Uptake ◽  
Pyruvate Dehydrogenase ◽  
Temporal Relationship ◽  
Glycogen Synthesis ◽  
Glucose Flux ◽  
Hepatic Glucose ◽  
Ad Libitum ◽  
Time Courses

A comparison was made between the time courses of restoration of pyruvate dehydrogenase activities, fructose 2,6-bisphosphate concentrations and lipogenic rates, together with net hepatic glucose flux and glycogen synthesis/deposition in livers of 48 h-starved rats provided with laboratory chow ad libitum for up to 24 h. Increased glycogenesis, lipogenesis and net glucose uptake were observed after 1 h of re-feeding, preceding re-activation of pyruvate dehydrogenase, which occurred after 3-4 h. Increased concentrations of fructose 2,6-bisphosphate were only observed after 5-6 h. The implication of the temporal relationship between these parameters is discussed.

scholarly journals The modes of action of toxic agents: II. Factors influencing the toxicities of mercury compounds to certain Crustacea

1957 ◽  
Vol 36 (3) ◽  
pp. 459-472 ◽  
Author(s):  
E. D. S. Corner ◽  
B. W. Sparrow
Keyword(s):  
Mercuric Chloride ◽  
Homologous Series ◽  
Secondary Compounds ◽  
Artemia Salina ◽  
Methyl Ethyl ◽  
Mercuric Iodide ◽  
Mercury Compounds ◽  
Factors Influencing ◽  
Toxic Agents ◽  
Primary Compounds

A study has been made of the toxicities of mercuric chloride, mercuric iodide and methyl-, ethyl-, n-propyl-, n-butyl-, n-amyl-, iso-propyl-, iso-amyl- and phenylmercuric chlorides to larvae of the crustaceans Artemia salina and Elminins modestus. With both species it has been found that all the mercury compounds are more toxic than mercuric chloride, that primary alkylmercuric chlorides are more toxic than the corresponding secondary compounds, and that as the homologous series of primary compounds is ascended, toxicities increase. In addition, it has been found that Elminius is much more readily poisoned than Artemia by each mercury compound, and that differences between the toxicities of the poisons to Elminius are much smaller than corresponding differences observed in experiments with Artemia.

Hexokinase II partial knockout impairs exercise-stimulated glucose uptake in oxidative muscles of mice

2003 ◽  
Vol 285 (5) ◽  
pp. E958-E963 ◽  
Author(s):  
Patrick T. Fueger ◽  
Sami Heikkinen ◽  
Deanna P. Bracy ◽  
Carlo M. Malabanan ◽  
R. Richard Pencek ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
High Glucose ◽  
Vastus Lateralis ◽  
Oxidative Capacity ◽  
Muscle Membrane ◽  
Moderate Exercise ◽  
Hexokinase Ii ◽  
Glucose Flux ◽  
Glucose Metabolic Rate

Muscle glucose uptake (MGU) is distributively controlled by three serial steps: delivery of glucose to the muscle membrane, transport across the muscle membrane, and intracellular phosphorylation to glucose 6-phosphate by hexokinase (HK). During states of high glucose fluxes such as moderate exercise, the HK activity is of increased importance, since augmented muscle perfusion increases glucose delivery, and increased GLUT4 at the cell membrane increases glucose transport. Because HK II overexpression augments exercise-stimulated MGU, it was hypothesized that a reduction in HK II activity would impair exercise-stimulated MGU and that the magnitude of this impairment would be greatest in tissues with the largest glucose requirement. To this end, mice with a HK II partial knockout ( HK+/–) were compared with their wild-type control (WT) littermates during either sedentary or moderate exercise periods. Rg, an index of glucose metabolism, was measured using 2-deoxy-[3H]glucose. No differences in glucose metabolism were detected between sedentary groups. The increase in Rgdue to exercise was impaired in the highly oxidative heart and soleus muscles of HK+/–compared with WT mice (7 ± 10 vs. 29 ± 9 and 8 ± 3 vs. 25 ± 7 μmol · 100 g–1· min–1, respectively). However, the increase in Rgdue to exercise was not altered in gastrocnemius and superficial vastus lateralis muscles in HK+/–and WT mice (8 ± 2 vs. 12 ± 3 and 5 ± 2 vs. 8 ± 2 μmol · 100 g–1· min–1, respectively). In conclusion, MGU is impaired by reductions in HK activity during exercise, a physiological condition characterized by high glucose flux. This impairment is critically dependent on the tissue's glucose metabolic rate and correlates with tissue oxidative capacity.

scholarly journals Factors Influencing the Determination of Colloid Osmotic Pressure of Plasma

1983 ◽  
Vol 5 (4) ◽  
pp. 405-412 ◽  
Author(s):  
Kenju MIKI ◽  
Sueko SAGAWA ◽  
Keizo SHIRAKI
Keyword(s):  
Osmotic Pressure ◽  
Colloid Osmotic Pressure ◽  
Factors Influencing

Muscle net glucose uptake and glucose kinetics after endurance training in men

1999 ◽  
Vol 277 (1) ◽  
pp. E81-E92 ◽  
Author(s):  
B. C. Bergman ◽  
G. E. Butterfield ◽  
E. E. Wolfel ◽  
G. D. Lopaschuk ◽  
G. A. Casazza ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Endurance Training ◽  
Power Output ◽  
Whole Body ◽  
Glucose Disposal ◽  
Moderate Intensity ◽  
Active Muscle ◽  
Glucose Kinetics ◽  
Glucose Flux

We evaluated the hypotheses that alterations in glucose disposal rate (Rd) due to endurance training are the result of changed net glucose uptake by active muscle and that blood glucose is shunted to working muscle during exercise requiring high relative power output. We studied leg net glucose uptake during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption (V˙o 2 peak)] and after training [65% pretrainingV˙o 2 peak, same absolute workload (ABT), and 65% posttrainingV˙o 2 peak, same relative workload (RLT)]. Nine male subjects (178.1 ± 2.5 cm, 81.8 ± 3.3 kg, 27.4 ± 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times a week at 75%V˙o 2 peak. The power output that elicited 66.0 ± 1.1% ofV˙o 2 peak before training elicited 54.0 ± 1.7% after training. Whole body glucose Rd decreased posttraining at ABT (5.45 ± 0.31 mg ⋅ kg−1 ⋅ min−1at 65% pretraining to 4.36 ± 0.44 mg ⋅ kg−1 ⋅ min−1) but not at RLT (5.94 ± 0.47 mg ⋅ kg−1 ⋅ min−1). Net glucose uptake was attenuated posttraining at ABT (1.87 ± 0.42 mmol/min at 65% pretraining and 0.54 ± 0.33 mmol/min) but not at RLT (2.25 ± 0.81 mmol/min). The decrease in leg net glucose uptake at ABT was of similar magnitude as the drop in glucose Rd and thus could explain dampened glucose flux after training. Glycogen degradation also decreased posttraining at ABT but not RLT. Leg net glucose uptake accounted for 61% of blood glucose flux before training and 81% after training at the same relative (65%V˙o 2 peak) workload and only 38% after training at ABT. We conclude that 1) alterations in active muscle glucose uptake with training determine changes in whole body glucose kinetics; 2) muscle glucose uptake decreases for a given, moderate intensity task after training; and 3) hard exercise (65%V˙o 2 peak) promotes a glucose shunt from inactive tissues to active muscle.

scholarly journals Determination of muscle-specific glucose flux using radioactive stereoisomers and microdialysis

2001 ◽  
Vol 280 (1) ◽  
pp. E187-E192 ◽  
Author(s):  
David A. MacLean ◽  
Steven M. Ettinger ◽  
Lawrence I. Sinoway ◽  
Kathryn F. Lanoue
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Human Subjects ◽  
Vastus Lateralis ◽  
Control Period ◽  
Tissue Level ◽  
Ringer Solution ◽  
Vastus Lateralis Muscle ◽  
Internal Reference ◽  
Glucose Flux

The purpose of the present study was to evaluate a novel approach for determining skeletal muscle-specific glucose flux using radioactive stereoisomers and the microdialysis technique. Microdialysis probes were inserted into the vastus lateralis muscle of human subjects and perfused (4 μl/min) with a Ringer solution containing small amounts of radioactived- and l-glucose as the internal reference markers for determining probe recovery as well as varying concentrations of insulin (0–10 μM). The rationale behind this approach was that both stereoisomers would be equally affected by the factors that determine probe recovery, with the exception ofl-glucose, which is nonmetabolizable and would not be influenced by tissue uptake. Therefore, any differences in the probe recovery ratios between the d- andl-stereoisomers represent changes in skeletal muscle glucose uptake directly at the tissue level. There were no differences in probe recovery between the d- (42.3 ± 3.5%) andl- (41.2 ± 3.5) stereoisomers during the control period (no insulin), which resulted in a D/L ratio of 1.04 ± 0.03. However, during insulin perfusion (1 μM), The D/L ratio increased to 1.62 ± 0.08 and 1.58 ± 0.07 ( P< 0.05) during the two collection (0–15 and 15–30 min) periods, respectively. This was accomplished solely by an increase ( P < 0.05) in d-glucose probe recovery, asl-glucose probe recovery remained unchanged. In a second set of experiments, the perfusion of 10 μM insulin did not increase the D/L ratio (1.40 ± 0.11) above that observed during 1.0 μM (1.41 ± 0.07) insulin perfusion. These data suggest that this method is sufficiently sensitive to detect differences in insulin-stimulated glucose uptake; thus the use of radioactive stereoisomers in conjunction with the microdialysis technique provides a novel and useful technique for determining tissue-specific glucose flux and insulin sensitivity.

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