Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Incubation of isolated rat epididymal fat cells is associated with the accumulation of adenosine in the incubation medium. To more clearly define the effect of adenosine on lipolysis, isolated rat epididymal adipocytes were studied with the perifusion system. Various combinations of epinephrine, adenosine, and adenosine deaminase were perifused through the adipocytes. Exogenous adenosine, 0.001-10.0 muM, had no discernible influence upon unstimulated lipolysis; but exogenous adenosine inhibited epinephrine-sensitive lipolysis in a concentration-dependent manner. Cells perifused with 0.3 muM epinephrine plus 0.001 muM adenosine did not show any impairment of the lipolytic response to 0.3 muM epinephrine alone. Adenosine, 0.01 muM, inhibited the response to epinephrine by 50%; response to 0.3 muM epinephrine plus 0.1 muM adenosine was similar to the basal rate. Perifusion with adenosine deaminase significantly increased basal lipolysis to 30% of the epinephrine response. Adenosine deaminase and epinephrine were synergistic in stimulating lipolysis to 180% of the response to epinephrine alone. Isolated fat cells were incubated for 30 min, and the cell-free used medium was perifused through fresh fat cells. Epinephrine in used medium was less effective in promoting lipolysis than epinephrine in fresh buffer. High-pressure liquid chromatography identified adenosine in the used medium. Bovine serum albumin possessed adenosine deaminase activity but accounted for negligible conversion of adenosine to inosine. Adenosine is shown to have a modulating effect upon basal and hormone-stimulated lipolysis in the perifusion system. Sufficient endogenous adenosine (<0.01 muM) is present to maximally affect basal lipolysis. Hormone-stimulated lipolysis, although inhibited somewhat by endogenous adenosine, requires the addition of exogenous adenosine for complete inhibition.
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PMID:Perifusion of isolated rat adipose cells. Modulation of lipolysis by adenosine. 87 2

The present study was conducted to determine the influence of dibutyryl-cAMP (dbcAMP), epinephrine, ractopamine and clenbuterol on insulin binding to porcine adipocytes. Dibutyryl-cAMP decreased insulin binding to swine adipocytes by 40 and 20% at 1.8 and 25.8 ng insulin/ml, respectively. Ractopamine and clenbuterol directly reduced insulin binding at the low insulin concentration and decreased binding at high insulin concentrations in the presence of adenosine deaminase. Scatchard analysis suggested that the reduction of insulin binding was due to a decrease in receptor number. Epinephrine alone did not influence insulin binding. In the presence of theophylline, epinephrine decreased binding at both low and high insulin concentrations; however, ractopamine plus theophylline decreased binding only at the low insulin concentration. Clenbuterol did not affect insulin binding in the presence of theophylline. Propranolol blocked the inhibitory effect of epinephrine on insulin binding. These beta-adrenergic agonists can inhibit insulin binding and, thus, antagonize insulin action in swine adipocytes.
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PMID:Decreased insulin binding to porcine adipocytes in vitro by beta-adrenergic agonists. 197 48

Adipose tissue lipolytic activity is increased in endurance-trained subjects, but little is known about the mechanisms of this increase. To understand more fully the mechanisms involved and to discover whether sex-related differences exist, biopsies of fat were performed in the periumbilical region of 20 sedentary subjects (10 women (W) and 10 men (M)) and 20 trained subjects (10 W, 10 M); the in vitro response to epinephrine of the collagenase-isolated fat cells was studied. Glycerol release, chosen as an adipocyte lipolysis indicator, was measured by bioluminescence. Dose-response curves with epinephrine (alpha 2 and beta agonist), with isoproterenol (beta agonist) and epinephrine + propranolol and adenosine deaminase, were studied. Epinephrine-induced lipolysis was enhanced in trained subjects and this was due to an increased efficiency of the beta-adrenergic pathway. However, differences were found between the two sexes. In trained men, the lipolysis increase resulted from the enhancement of the beta-adrenergic pathway efficiency without any significant decrease in the alpha 2-adrenergic pathway efficiency. In trained women, the lipolysis increase was not only due to the enhancement of the beta-adrenergic pathway efficiency (which was greater than in trained men), but also to a significant decrease in the alpha 2-adrenergic pathway efficiency. Despite the decrease, the alpha 2-adrenergic pathway remained more efficient in trained women than in trained men, as was the case in sedentary subjects. It is concluded that endurance training led to better lipid mobilization and that this effect seemed greater in women than in men.
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PMID:Lipolytic response of adipocytes to epinephrine in sedentary and exercise-trained subjects: sex-related differences. 258 71

Investigations were carried out to demonstrate the function and the possible advantage of the interplay between beta 1 and alpha 2 adrenoceptor sites in the regulation of human subcutaneous fat-cell lipolysis. alpha 2 and beta adrenoceptor binding studies were conducted with antagonist radioligands and revealed that alpha 2-adrenoceptors ([3H]yohimbine and [3H]rauwolscine binding sites) are more numerous than beta 1-adrenoceptors ([3H]dihydroalprenolol and [3H]CGP-12177 binding sites) in human fat-cell membranes. Physiological agonists epinephrine and norepinephrine competed with [3H]-ligand sites with a higher affinity for alpha 2 sites than for beta 1 sites. Epinephrine exhibited a higher affinity than norepinephrine for the alpha 2 sites; the two amines had the same affinity for beta 1 sites. In lipolysis studies conducted in the absence of adenosine deaminase the beta lipolytic action of the biological amines predominated; after alpha 2-adrenoceptor blockade by yohimbine or idazoxan, the amines exhibited an intrinsic activity similar to that of isoproterenol. When adenosine was prevented from accumulating in the incubation medium by inclusion of adenosine deaminase, low concentrations of epinephrine and norepinephrine preferentially exerted an antilipolytic action. We conclude that: he lipolytic response in abdominal human subcutaneous fat cells to physiological amines results from the interplay between beta 1-and alpha 2-adrenoceptor stimulation; alpha 2 adrenoceptors, with their higher number and higher affinity for the physiological amines, and the adrenoceptor population involved at the lowest (i.e. physiological) concentrations of the amines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that epinephrine acts preferentially as an antilipolytic agent in abdominal human subcutaneous fat cells: assessment by analysis of beta and alpha 2 adrenoceptor properties. 300 59

Epinephrine, norepinephrine and isoproterenol completely inhibited insulin-stimulated 2-deoxyglucose uptake by rat adipocytes, but only when adenosine was prevented from accumulating in the incubation medium by addition of adenosine deaminase. Basal uptake rates were not affected. The effects were not observed in the presence of adenosine deaminase plus N6-phenylisopropyl adenosine (a non-metabolizable adenosine analogue), suggesting that it is the lowered adenosine level rather than the presence of the enzyme itself which allows the catecholamines to inhibit insulin action. The inhibitory effects of the catecholamines were blocked by propranolol but not phentolamine, suggesting that they are mediated via beta-adrenergic receptors.
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PMID:Catecholamines inhibit insulin-stimulated glucose transport in adipocytes, in the presence of adenosine deaminase. 613 Sep 79

1. Adipocytes isolated from epididymal fat-pads of fed rats were incubated with different concentrations of glucagon, insulin, adrenaline and adenosine deaminase, and the effects of these agents on the ;initial' activity of acetyl-CoA carboxylase in the cells were studied. 2. Glucagon (at concentrations between 0.1 and 10nm) inhibited acetyl-CoA carboxylase activity. Maximal inhibition was approx. 70% of the ;control' activity in the absence of added hormone, and the concentration of hormone required for half-maximal inhibition was 0.3-0.5nm-glucagon. 3. Incubation of cells with adenosine deaminase resulted in a similar inhibition of acetyl-CoA carboxylase activity. Preincubation of adipocytes with adenosine deaminase did not alter either the sensitivity of carboxylase activity to increasing concentrations of glucagon or the maximal extent of inhibition. 4. Adrenaline inhibited acetyl-CoA carboxylase to the same extent as glucagon. Preincubation of the cells with glucagon did not alter the sensitivity of enzyme activity to adrenaline or the degree of maximal inhibition. 5. Insulin activated the enzyme by 70-80% of ;control' activity. Preincubation of the cells with glucagon did not alter the concentration of insulin required to produce half the maximal stimulatory effect (about 12muunits of insulin/ml). The effects of insulin and glucagon appeared to be mediated completely independently, and were approximately quantitatively similar but opposite. These characteristics resulted in the mutual cancellation of the effects of the two hormones when they were both present at equally effective concentrations. 6. The implications of these findings with regard to current concepts about the mechanism of regulation of acetyl-CoA carboxylase and to the regulation of the enzyme in vivo are discussed.
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PMID:Inhibition of acetyl-CoA carboxylase activity in isolated rat adipocytes incubated with glucagon. Interactions with the effects of insulin, adrenaline and adenosine deaminase. 613 71

Adrenaline and adenosine deaminase decreased the rate of phosphate uptake in isolated rat adipocytes. This effect was inhibited by N6(phenylisopropyl)adenosine. The rate of uptake was decreased by one third if the rats were given triiodothyronine prior to killing. In fat cells from hypothyroid rats, phosphate uptake was not sensitive to adrenaline. Sensitivity was restored by exogenous adenosine deaminase.
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PMID:Regulation of phosphate uptake in rat adipocytes by adenosine, catecholamines and thyroid hormones. 723 35

White and brown rat adipocytes have been permeabilised by repeated exposure of the cells in suspension to high voltage electrical discharges. The resulting preparations were permeable to low molecular weight materials, e.g., cyclic AMP, propidium iodide, and were stable in suspension with little evidence of rapid resealing, or of gross damage to the cell membrane. Leakage of lactate dehydrogenase was not markedly enhanced except at voltages in excess of 2 kV cm-1 for brown adipocytes. Exogenously-added cyclic AMP stimulated lipolysis (measured as glycerol release) in the electropermeabilised adipocytes far more effectively than in intact adipocytes. In brown, but not in white, adipocytes this effect was enhanced by addition of millimolar ATP. The EC50 for stimulation of glycerol release by cyclic AMP was 0.2 microM in electropermeabilised brown adipocytes, and 2 microM and 40 microM in electropermeabilised white adipocytes obtained from weanling and adult rats respectively. The effect of cyclic AMP on lipolysis was enhanced by addition of an inhibitor of cyclic AMP phosphodiesterases and was reduced by addition of 5'-AMP, adenosine or inosine (in brown adipocytes). Addition of adenosine deaminase caused a small, but significant, enhancement of cyclic AMP-driven lipolysis. Catecholamine-driven lipolysis was observed in electropermeabilised brown and white adipocytes, especially in the presence of GTP. Adrenaline-, and to a lesser extent cyclic AMP-, driven lipolysis in electropermeabilised white adipocytes was inhibited by insulin. This effect of insulin was not enhanced by addition of GTP or of a metabolically stable GTP analogue. The results obtained establish the electropermeabilised preparation as suitable for analysis of signal transduction pathways in white and brown adipocytes.
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PMID:Studies on signal transduction mechanisms for adrenaline-driven lipolysis in white and brown adipocytes. 816 54

Twelve control (C) and 12 prenatally androgenized (PA) lactating (L) first-calf heifers and five (two C and three PA) similar, nonlactating (NL) heifers were used to assess the effects of PA and L on the metabolic activity of s.c. adipose tissue (AT). Heifers were fed an 85% concentrate diet, and their calves were weaned at 112 +/- 1 d of age. Adipose tissue was biopsied at approximately 77 d (period 1, during lactation for L heifers) and 126 d (period 2, after L heifers had calves weaned) postpartum. The NL heifers gained .22 kg/d faster (P = .20) and had greater fat deposition than L heifers during period 1. The PA heifers were fatter and gained 14.6% faster than C heifers during lactation. Epinephrine (E) and norepinephrine (NE) increased in vitro fatty acid (FA) release 25 (P < .01) and 15% (P < .06), respectively, above basal rates. Near-maximal release of FA, as estimated by stimulation with E plus theophylline plus adenosine deaminase (ETAD), was 73% (4,110 vs 2,379 +/- 161 nEq/[2 h.100 mg of tissue]; P < .01) above basal rates. Basal FA release was unaffected, but ETAD-stimulated rates were decreased (P < .04; 4,430 +/- 246 vs 3,789 +/- 209 nEq/[2 h.100 mg of tissue]) by PA. Stimulation of FA release by E (P = .22) or NE (P = .31) did not differ between C and PA. For NL heifers, PA decreased (P < .02) FA release, which corresponded with their greater fat deposition, but PA did not affect L heifers (PA x L interaction, P = .14). The content of NEFA in s.c. AT (pool size) was 34% greater (P < .01) during period 2 than during period 1. Pool size was not affected (P = .72) by NE but was increased by E (1,628 vs 1,777 +/- 92 nEq/100 mg of tissue; P < .05) and ETAD (1,628 vs 2,176 +/- 93 nEq/100 mg of tissue; P < .01). For L heifers, PA tended (P < .07) to increase incorporation of acetate into FA during period 1. Thus, PA resulted in subtle increases in lipogenesis and decreases in lipolysis during the first lactation-weaning cycle that were consistent with greater rates of gain and fat deposition.
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PMID:Effects of prenatal androgenization and lactation on adipose tissue metabolism in finishing single-calf heifers. 925 May 10

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