Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentration of insulin that produces half-maximal stimulation of glycolysis in stripped soleus muscle preparations is decreased from approximately 100-10 muunits/ml by the presence of adenosine deaminase in the incubation medium. This suggests that adenosine decreases insulin sensitivity. The effect of the deaminase is abolished by addition of the adenosine analogue, N6-phenylisopropyladenosine which is not metabolised by the deaminase. The effect of the deaminase in isolated soleus muscle is similar to that of a period of physical training of the rat.
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PMID:Effect of adenosine deaminase and an adenosine analogue on insulin sensitivity in soleus muscle of the rat. 634 99

Effects of adenosine deaminase and glucagon on insulin-stimulated 2-deoxyglucose uptake by rat adipocytes are reported. (1) Adenosine deaminase (10 micrograms/ml) caused a rightward shift in the dose-response curve for the stimulation by insulin of 2-deoxyglucose uptake, but the enzyme did not alter either the basal or the maximally insulin-stimulated uptake rate. (2) In adipocytes obtained from 24 h-starved rats, glucagon inhibited the effect of insulin on 2-deoxyglucose uptake in the presence (but not in the absence) of adenosine deaminase. Basal uptake rates were unaffected. (3) Glucagon inhibited insulin-stimulated 2-deoxyglucose uptake to a greater extent in cells isolated from starved rats than in cells from fed rats. (4) Adipocytes isolated from fed and from starved rats did not differ in their capacity for degradation of 125I-labelled glucagon. The results suggest that adenosine and glucagon are regulators of insulin action in adipose tissue.
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PMID:Glucagon inhibition of insulin-stimulated 2-deoxyglucose uptake by rat adipocytes in the presence of adenosine deaminase. 634 92

Adenosine and its analogue N6-phenylisopropyladenosine stimulated pyruvate dehydrogenase activity of isolated rat adipocytes. Maximal stimulation was obtained with concentrations between 50 and 100 mu M, with the effect decreasing at higher concentrations. The effects of insulin on this enzyme was modified by adenosine. The concentration of insulin (10 mu units/ml) that produced almost half-maximal stimulation, had little or no effect, when adenosine deaminase was present. Adenosine also enhanced the effect of suboptimal but not optimal concentrations of insulin. Thus, the mechanism of adenosine action on adipocyte pyruvate dehydrogenase could in some way be similar or related to that of insulin.
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PMID:Effect of adenosine on insulin activation of rat adipocyte pyruvate dehydrogenase. 638 62

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.
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PMID:Reversal of dietary-induced insulin resistance in muscle of the rat by adenosine deaminase and an adenosine-receptor antagonist. 639 73

Exposure to phospholipase C increased the incorporation of [32P]Pi into phosphatidate, CMP-phosphatidate and phosphatidylinositol in rat adipose tissue and isolated adipocytes. A similar effect was observed in response to insulin and oxytocin. Theophylline, 3-isobutyl-1-methylxanthine and adenosine deaminase decreased [32P]Pi incorporation, and adenosine and N6-phenylisopropyladenosine reversed these effects. As with insulin, exposure of adipose tissue to phospholipase C stimulated oxidation of glucose, pyruvate and leucine and activated pyruvate dehydrogenase. Oxytocin and adenosine also mimicked the effects of insulin on leucine oxidation and pyruvate dehydrogenase. However, only insulin stimulated glycogen synthase activity, indicating that the regulation of synthase may be achieved by intracellular events distinct from those regulating changes in phospholipid metabolism, sugar transport and mitochondrial enzyme activities. It is postulated that exposure to phospholipase C forms diacylglycerol, which is phosphorylated to yield phosphatidate. The increased labelling of CMP-phosphatidate and phosphatidylinositol results from the conversion of phosphatidate into these lipids. The correlation between the effects of phospholipase C on phosphatidate synthesis and changes in adipose-tissue metabolism suggests the possibility that increased phosphatidate may directly or indirectly produce changes in membrane transport and enzyme activities. The pattern of phospholipid labelling produced by insulin, adenosine and oxytocin suggests that these stimuli may also increase phosphatidate synthesis, and, if so, changes in phospholipid metabolism could account for some of the metabolic actions of these stimuli.
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PMID:Phosphatidic acid and phosphatidylinositol labelling in adipose tissue. Relationship to the metabolic effects of insulin and insulin-like agents. 641 Oct 68

Insulin action and insulin binding in isolated rat fat cells incubated with adenosine or adenosine deaminase were studied. Adenosine enhanced the effects of insulin on glucose transport and glucose metabolism. The nucleoside shifted the concentration-response curves of insulin-stimulated D-[3-3H]glucose incorporation into total lipids, and of D-[U-14C]glucose conversion to fatty acids to smaller insulin concentrations. In addition, the maximal response of the fatty acid synthesis was increased. Insulin sensitivity and maximal response to insulin of the glucose transport system, as assessed by the rate of uptake of 2-deoxyglucose and 3-O-methylglucose, were increased by adenosine. The adenosine derivative N6-phenylisopropyladenosine similarly enhanced deoxyglucose transport in the presence of insulin. However, insulin binding was not affected by adenosine. The results suggest that adenosine modulates insulin action at a step distal from the insulin receptor, and before, or at, the glucose transport system.
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PMID:Modulation of insulin sensitivity by adenosine. Effects on glucose transport, lipid synthesis, and insulin receptors of the adipocyte. 675 15

Adipocytes from streptozotocin-diabetic rats are approximately 50-times more sensitive to the lipolytic action of glucagon. This change is only perceived in the presence of a small quantity of adenosine deaminase which itself has little effect on basal lipolysis. Insulin treatment restores glucagon sensitivity to normal.
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PMID:Streptozotocin diabetes results in increased responsiveness of adipocyte lipolysis to glucagon. 684 Feb 81

The removal of extracellular, endogenously produced adenosine in isolated rat adipocytes by treatment with adenosine deaminase enhanced their responsiveness to various lipolytic agents, i.e. the response to catecholamines, glucagon, LH, TSH, and cholera toxin was elicited at concentrations that were 10-500 times lower than those required for the stimulation of lipolysis in untreated cells in vitro. The removal of adenosine from intact fat cells largely potentiated the isoproterenol-stimulated increase in cAmP level. However, a similar treatment of undissociated segments of adipose tissue failed to influence further the response to isoproterenol. These results strongly suggest that in the intact adipose tissue, adenosine and related nucleosides are absent and do not function as modulators of adenylate cyclase or lipolysis. Under these circumstances the estimated "low" physiological concentrations of the neurotransmitters in the adipose tissue are able to modulate lipid mobilization. Previous studies have shown that insulin failed to inhibit lipolysis, induced by micromolar norepinephrine concentrations, in adenosine-free adipocytes. The present study demonstrates that at physiological catecholamine concentrations, insulin is a potent antilipolytic agent.
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PMID:Evaluation of adenosine or related nucleosides as physiological regulators of lipolysis in adipose tissue. 704 12

Maturity-onset diabetes of the young (MODY) is a model for genetic studies of non-insulin-dependent diabetes mellitus. We have identified 15 MODY families in which diabetes is not the result of mutations in the glucokinase gene. This cohort of families will be useful for identifying other diabetes-susceptibility genes. Nine other candidate genes potentially implicated in insulin secretion or insulin action have been tested for linkage with MODY in these families, including glucokinase regulatory protein, hexokinase II, insulin receptor substrate 1, fatty acid-binding protein 2, glucagon-like peptide-1 receptor, apolipoprotein C-II, glycogen synthase, adenosine deaminase (a marker for the MODY gene on chromosome 20), and phosphoenolpyruvate carboxykinase. None of these loci showed evidence for linkage with MODY, implying that mutations in these genes do not make a major genetic contribution to the development of MODY. In addition to these linkage analyses, one or two affected subjects from each family were screened for the presence of the A to G mutation at nucleotide 3,243 of the mitochondrial tRNA(Leu(UUR)) gene. This mutation was not found in any of these subjects. Finally, we report the localization of the gene encoding the regulatory protein of glucokinase to chromosome 2, band p22.3 and the identification of a restriction fragment length polymorphism at this locus.
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PMID:Search for a third susceptibility gene for maturity-onset diabetes of the young. Studies with eleven candidate genes. 750 74

The change in transmembrane potential of rat adipocytes was measured using the fluorescent probe 3,3'-diethylthiadicarbocyanine iodide, diS-C2-(5). The method was calibrated by altering the potassium ion concentration while keeping the sum of potassium and sodium ions at a constant concentration of 153 mM (Bailey et al: Bioelectrochem. Bioenergetics 21:333-42, 1989). Two insulin-mimetic agents, phospholipase C from Clostridium perfringens and concanavalin A, induced a dose dependent hyperpolarization of rat epididymal adipocytes, like insulin. Removal of endogenous adenosine with adenosine deaminase or adenosine receptor blockade with isobutylmethylxanthine following the initiation of insulin-induced hyperpolarization resulted in depolarization. These same agents induced hyperpolarization of -6 to -8 mV when added without insulin. The replacement of adenosine with its analogue, N6-phenylisopropyladenosine, plus insulin depolarized the cells toward the transmembrane potential established by insulin, -2.0 mV. These studies suggest that adenosine receptor occupancy is required to maintain insulin-induced hyperpolarization.
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PMID:Membrane potential of rat adipocytes: effect of phospholipase C, concanavalin A, and adenosine. 751 7


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