scholarly journals Reversal of dietary-induced insulin resistance in muscle of the rat by adenosine deaminase and an adenosine-receptor antagonist

1984 ◽  
Vol 224 (1) ◽  
pp. 327-330 ◽  
Author(s):  
L Budohoski ◽  
R A J Challiss ◽  
G J Cooney ◽  
B McManus ◽  
E A Newsholme
Keyword(s):  
Insulin Resistance ◽  
Drinking Water ◽  
Receptor Antagonist ◽  
Adenosine Deaminase ◽  
Soleus Muscle ◽  
Adenosine Receptor ◽  
Maximum Response ◽  
Insulin Resistant ◽  
Adenosine Receptor Antagonist ◽  
Young Rats

Transfer of young rats from a maintenance diet to a breeding diet plus 10% sucrose in the drinking water for 4 weeks caused the development of insulin resistance. Inclusion of the enzyme adenosine deaminase or the adenosine-receptor antagonist 8-phenyltheophylline caused a marked increase in the sensitivity of the soleus-muscle strips isolated from the diet-induced insulin-resistant rats: the concentration of insulin giving 50% of maximum response of glycolysis shifted from 500 to less than 20 microunits/ml.

scholarly journals Effects of an adenosine-receptor antagonist on insulin-resistance in soleus muscle from obese Zucker rats

1984 ◽  
Vol 221 (3) ◽  
pp. 915-917 ◽  
Author(s):  
R A Challis ◽  
L Budohoski ◽  
B McManus ◽  
E A Newsholme
Keyword(s):  
Insulin Resistance ◽  
Receptor Antagonist ◽  
Adenosine Receptor ◽  
Adenosine Receptors ◽  
Glucose Utilization ◽  
Glycogen Synthesis ◽  
Zucker Rats ◽  
Adenosine Receptor Antagonist ◽  
Obese Rats ◽  
Obese Zucker Rats

The decreased sensitivity of glycolysis to insulin seen in isolated soleus muscles from genetically obese Zucker rats was abolished by addition of the adenosine-receptor antagonist 8-phenyltheophylline to the incubation medium; 8-phenyltheophylline had no effect on the sensitivity of glycogen synthesis to insulin. These findings suggest that changes in the sensitivity of glucose utilization by muscles of genetically obese rats may be explained, in part, by a modification in either the concentration of adenosine or the affinity of adenosine receptors in skeletal muscle.

CPX, a selective A1-adenosine-receptor antagonist, regulates intracellular pH in cystic fibrosis cells

1995 ◽  
Vol 269 (1) ◽  
pp. C226-C233 ◽  
Author(s):  
V. Casavola ◽  
R. J. Turner ◽  
C. Guay-Broder ◽  
K. A. Jacobson ◽  
O. Eidelman ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Receptor Antagonist ◽  
Intracellular Ph ◽  
Adenosine Receptor ◽  
Ph Regulation ◽  
Cystic Fibrosis Transmembrane Regulator ◽  
Wild Type ◽  
A1 Adenosine Receptor ◽  
Adenosine Receptor Antagonist ◽  
Cystic Fibrosis Transmembrane

The selective A1-adenosine-receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (CPX), has been reported to activate Cl- efflux from cystic fibrosis cells, such as pancreatic CFPAC-1 and lung IB3 cells bearing the cystic fibrosis transmembrane regulator(delta F508) mutation, but has little effect on the same process in cells repaired by transfection with wild-type cystic fibrosis transmembrane regulator (O. Eidelman, C. Guay-Broder, P. J. M. van Galen, K. A. Jacobson, C. Fox, R. J. Turner, Z. I. Cabantchik, and H. B. Pollard. Proc. Natl. Acad. Sci. USA 89: 5562-5566, 1992). We report here that CPX downregulates Na+/H+ exchange activity in CFPAC-1 cells but has a much smaller effect on cells repaired with the wild-type gene. CPX also mildly decreases resting intracellular pH. In CFPAC-1 cells, this downregulation is dependent on the presence of adenosine, since pretreatment of the cells with adenosine deaminase blocks the CPX effect. We also show that, by contrast, CPX action on these cells does not lead to alterations in intracellular free Ca2+ concentration. We conclude that CPX affects pH regulation in CFPAC-1 cells, probably by antagonizing the tonic action of endogenous adenosine.

Synthesis of an o-Nitrobenzyl Attached A1 Adenosine Receptor Antagonist, a Prodrug Approach.

ChemInform ◽  
2003 ◽  
Vol 34 (47) ◽  
Author(s):  
HeXi Chang ◽  
Carol Ensinger ◽  
Robert D. McCargar ◽  
Bruno M. Vittimberga
Keyword(s):  
Receptor Antagonist ◽  
Adenosine Receptor ◽  
A1 Adenosine Receptor ◽  
Adenosine Receptor Antagonist

The adenosine receptor blocker aminophylline increases anoxic ethanol excretion in crucian carp

1991 ◽  
Vol 261 (4) ◽  
pp. R1057-R1060 ◽  
Author(s):  
G. E. Nilsson
Keyword(s):  
Oxygen Consumption ◽  
Energy Consumption ◽  
Receptor Antagonist ◽  
Adenosine Receptor ◽  
Crucian Carp ◽  
Receptor Blocker ◽  
Carassius Carassius ◽  
Adenosine Receptor Antagonist ◽  
Crucian Carp Carassius Carassius

By depressing energy consumption, anoxia-tolerant animals are thought to compensate for a reduced ability to produce energy during anoxia. Adenosine is an inhibitory neuromodulator in vertebrates and, hence, has the potential ability to depress energy consumption. Ethanol is the main metabolic end product in anoxic Carassius, and the present study shows that the rate of ethanol excretion in anoxic crucian carp (Carassius carassius L.) can be increased threefold by treatment with the adenosine receptor antagonist aminophylline (75 mg/kg). By contrast, the same dose of aminophylline did not increase the rate of routine oxygen consumption during normoxia. It is hypothesized that adenosine acts as a metabolic depressant during anoxia in crucian carp.

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