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)

ACTH at levels as low as 0.05 mU/ml stimulated lipolysis, protein kinase and cyclic AMP accumulation in isolated fat cells from fed and fasted rats. Changes in cyclic AMP levels and in the protein kinase activity ratio were well correlated temporally. The protein kinase activity ratio was potentiated by adenosine deaminase. A sudden increase or decrease in either ACTH or dibutyryl cyclic AMP concentration was associated with a rapid and corresponding change in the rate of glycerol production. With ACTH, the changes in glycerol production were accompanied by appropriate changes in cyclic AMP levels. Actinomycin-D (10 UM) did not affect lipolysis or cyclic AMP accumulation activated by ACTH in fat cells.
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PMID:The correlation of cyclic AMP and protein kinase activity in adipocytes with lipolysis stimulated by ACTH: the effect of adenosine deaminase and actinomycin D. 21 72

Clonal lines, with either partial or total deficiency of adenine phosphoribosyltransferase (APRT) were derived from the WI-L2 long-term human lymphocyte line by selection for resistance to the adenine analogs 8-azaadenine or 2,6-diaminopurine. Resistance to 8-azaadenine also conferred resistance to 2,6 diaminopurine and vice versa. Cells with 30--40% of wild-type APRT activity were selected by resistance to 0.01 mM 2,6-diaminopurine or 1.40 mM 8-azaadenine. The APRT in the 8-azaadinine-resistant cells exhibited a four- to sevenfold increase in the apparent Km for adenine. Activities of three other purine reutilization and interconversion enzymes in the resistant cells, including hypoxanthine phosphoribosyltransferase (HPRT), adenosine kinase, and adenosine deaminase, were within the range of wild-type activities. The doubling times of the APRT-deficient cells in purine-free medium was not different from wild-type cells. The APRT in the 8-azaadenine-resistant cells did not have an altered mobility in glycerol gradients as compared to wild-type cells. The rate of purine synthesis de novo and intracellular levels of 5-phosphoribosyl-1-pyrophosphate were unchanged in the APRT-deficient cells as compared to WI-L2. The ability of the cells to reutilize exogenous adenine, however, was severely impaired.
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PMID:Purine reutilization and synthesis de novo in long-term human lymphocyte cell lines deficient in adenine phosphoribosyltransferase activity. 69 20

The stability over time for lipolysis in isolated human subcutaneous fat cells was investigated in 13 non-obese volunteers who underwent two gluteal fat biopsies under local anaesthesia at random intervals (mean 18 months). Glycerol release to the incubation medium was measured in the absence or the presence of lipolytic or antilipolytic adrenergic agents. The half-maximum effects (ED50) of norepinephrine, the non-selective beta-agonist isoprenaline and the selective alpha 2 agonist clonidine were determined and each had an intraindividual coefficient of variation of 7 per cent. The precision of the lipolysis assay, performed in duplicate, was 10 per cent. The coefficient of variation for lipolysis at the maximum effective concentrations of the agonists was between 20 per cent and 30 per cent. The addition of adenosine deaminase does not reduce the variability. In conclusion, the isolated human fat cell lipolysis assay shows some variability for maximum action of adrenergic agonists on lipolysis. However, there is a small variability in ED50 for such agents which indicates that the assay is well suited for determining drug sensitivity.
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PMID:Stability over time of adrenergic sensitivity in isolated human fat cells. 131 40

The objective was to study the control of lipolysis and to determine kinetic relationships between subcutaneous adipose tissue cyclic AMP concentrations and rates of lipolysis in primiparous dairy cows in late pregnancy and early lactation. Adipose tissue was biopsied from primiparous cows at -30, -15, -5, 5, 15, 30, and 60 d around parturition. Tissue was incubated with the following treatments: basal, no additions; isoproterenol at 10(-5) M; adenosine deaminase at 1 x 10(6) munits/ml; combined isoproteranol and adenosine deaminase; isoproteranol, adenosine deaminase, and 1 mM theophylline. Cyclic AMP was highest at .25 h and remained elevated for 2 h. Response of cyclic AMP at .25 h was 5-, 9-, 27-, and 38-fold for the four stimulatory treatments, respectively. Glycerol release at 2 h increased 3-, 2.3-, 2.7-, and 3-fold, respectively. Lipolysis was related logarithmically to cyclic AMP concentrations within and among treatments and times around parturition. Either logarithmic or Michaelis-Menten equations predicted similar maximum lipolysis but increased sensitivity to cyclic AMP in tissue from lactating compared with pregnant heifers. Thus, the sensitivity of response of lipolysis to cAMP may be increased in adipose tissue from first lactation cows. These relationships also may be useful in constructing and improving mechanistic models of adipose and whole animal metabolism.
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PMID:Quantitative relationships between cyclic adenosine-3',5'-monophosphate and lipolysis in adipose tissue during the peripartum period. 132 84

The rates of glycerol release in adipocytes isolated from nine identified adipose depots of sedentary or exercised guinea-pigs were measured in the presence of adenosine deaminase and 10(-9) to 10(-5) M noradrenaline and/or 1-1000 muunit/ml of bovine insulin. Twenty minutes of exercise increased the basal noradrenaline-stimulated rates of lipolysis in all depots, but these effects, and their interactions with in vitro application of the neurotransmitter differed between depots, showing that the long-lasting effects of exercise and the response to acute application of NA involve different mechanisms that may occur separately or together in different adipose depots. In general, large depots had the highest resting rates of lipolysis and the lowest responses to both noradrenaline and insulin, and lipolysis was only slightly different from the basal rate in adipocytes incubated with mixtures of the two agents. The two small intermuscular depots had the lowest unstimulated rates of lipolysis, but the fastest change and greatest maximum response to both agents. Noradrenaline-stimulated lipolysis was most effectively inhibited by small quantities of insulin in these depots. Different combinations of these properties were demonstrated in two smaller superficial depots, the mesenteric and omental depot, and in the cardiac depots. The data demonstrate the physiological inhomogeneity of both 'subcutaneous' and 'intra-abdominal' depots, and are consistent with the hypothesis that intermuscular adipose tissue interacts locally with adjacent muscle. Noradrenaline-stimulated lipolysis was more effectively inhibited by 100 muunit/ml insulin in adipocytes from the mesenteric and omental depot in those from any other site. A possible role for this property in the enlargement of this depot in hyperinsulinaemia in humans is proposed.
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PMID:The effects of noradrenaline and insulin on lipolysis in adipocytes isolated from nine different adipose depots of guinea-pigs. 183 17

Neuropeptide Y (NPY) and peptide YY (PYY) are regulatory peptides that have considerable sequence homology with pancreatic polypeptide. Because (a) NPY has been shown to be colocalized with noradrenaline in peripheral as well as central catecholaminergic neurons, and (b) alpha 2-adrenergic receptors of adipocytes play a major role in the regulation of lipolysis, we investigated the effect of NPY and PYY on isolated fat cells. In human fat cells NPY and PYY promoted a dose-dependent inhibition of lipolysis elicited by 2 micrograms/ml adenosine deaminase (removal of adenosine) whatever the lipolytic index used (glycerol or nonesterified fatty acids). In dog fat cells NPY and PYY inhibited adenosine deaminase-, isoproterenol- and forskolin-induced lipolysis. In humans and dogs the effects of NPY or PYY were abolished by treatment of cells with Bordetella pertussis toxin, clearly indicating the involvement of a Gi protein in the antilipolytic effects. This study indicates that, in addition to alpha 2-adrenergic agonists, NPY and PYY are also involved in the regulation of lipolysis in human and dog adipose tissue as powerful antilipolytic agents. Further studies are needed to characterize the pharmacological nature of the receptor mediating the inhibitory effect of NPY and PYY in fat cells.
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PMID:Neuropeptide Y and peptide YY inhibit lipolysis in human and dog fat cells through a pertussis toxin-sensitive G protein. 210 80

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

The relationships between cyclic AMP (cAMP) levels and glycerol release (lipolysis) were determined for isoproterenol and forskolin under varied conditions in the isolated fat cell of the rat. Prevention of the inhibitory action of endogenous adenosine [by adenosine deaminase (100 mU/ml) or theophylline (3.3 X 10(-4) M)] resulted in increased levels of cAMP and increased rates of lipolysis with forskolin. However, the relationship between cAMP levels and rates of lipolysis remained the same under all conditions. N6-phenylisopropyladenosine (PIA; an analog of adenosine) abolished the increase in cAMP level produced by isoproterenol (10(-7) M) or forskolin (10(-6) M) and the lipolytic response to forskolin. However, PIA failed to inhibit completely the lipolytic response to isoproterenol. Dose-response curves to isoproterenol were determined in the presence and absence of adenosine deaminase. PIA (10(-6) M) inhibited the increase in cAMP levels under both conditions. PIA also inhibited the lipolytic responses that were associated with increases in cAMP levels, i.e., high concentrations of isoproterenol alone and isoproterenol with adenosine deaminase. A plot of cAMP levels against corresponding rates of lipolysis for all conditions agreed with previous observations that the relationship for isoproterenol differs from that for forskolin. At any concentration of cAMP the corresponding lipolytic response was greater for isoproterenol than for forskolin. The possibility of a cAMP-independent lipolytic response was discussed.
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PMID:Quantitative differences in the cyclic AMP-lipolysis relationships for isoproterenol and forskolin. 285 46

The effects of adrenaline, noradrenaline, and of the alpha 2- and beta-selective agonists clonidine and isoproterenol were studied in fifteen obese subjects before and after 4 weeks of caloric restriction (300 cal day-1). Basal glycerol release averaged 1.4 mumol (10(6) cells)-1 (180 min)-1 before starvation and 2.8 mumol (10(6) cells)-1 (180 min)-1 during starvation (P less than or equal to 0.1). Before starvation adrenaline and noradrenaline caused a 2-3-fold increase of glycerol release. This lipolytic effect disappeared during starvation. An inhibitory effect of adrenaline was observed instead which was maximal at an adrenaline concentration of 1 mumol 1(-1) (P less than or equal to 0.05). The dose-response relationships of the alpha 2- and beta-selective agents clonidine and isoproterenol were not appreciably changed by caloric restriction. The increase of basal lipolytic rate and the reversal of adrenaline action seen during caloric restriction could be mimicked by removal of endogenous adenosine using adenosine deaminase (1.6 microgram ml-1). In addition, inclusion of N6-phenylisopropyladenosine (1 mumol 1(-1)) into the medium reverted the adrenaline-induced inhibition seen during caloric restriction. The results suggest that local modulators such as adenosine are of primary importance for the apparent change of responsiveness to adrenaline and noradrenaline seen during starvation of human fat cells in vitro.
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PMID:Adrenergic regulation of lipolysis in abdominal adipocytes of obese subjects during caloric restriction: reversal of catecholamine action caused by relief of endogenous inhibition. 285 98

Despite numerous reports of solubilization of adenosine A1 receptors, little progress has been made in isolating or purifying the receptor, owing to the extreme lability of the preparations. The present solubilization strategies recognized the possible role of endogenous adenosine to produce adenosine-receptor-N-protein complexes, which are intrinsically unstable, and instead attempted to use caffeine to solubilize free adenosine receptors, which might be more stable. Endogenous adenosine was removed from membranes by using adenosine deaminase along with GTP to accelerate the release of receptor-bound adenosine. The receptors were then occupied with caffeine and solubilized with 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulphonate (CHAPS) in the presence of glycerol. These soluble preparations exhibited the characteristics of free adenosine receptors. They bound the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPDPX) with high affinity to a single class of binding sites, which were insensitive to GTP. The binding activity was extremely stable, with a half-life of about 5 days at 4 degrees C; there was little change in either receptor number or affinity during 3 days at 4 degrees C. This methodology should greatly facilitate the characterization, isolation and purification of the adenosine A1 receptor.
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PMID:Solubilization of stable adenosine A1 receptors from rat brain. 293 Apr 58


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