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:4.6.1.1 (adenylate cyclase)
19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two children are described with congenital abnormalities (microcephaly, nystagmus, deafness, hepatomegaly) and the anomalous feature of triglyceride deposits in peripheral adipose tissue associated with severe malnutrition. Peripheral adipose tissue of one of these children displayed: (a) reduced sensitivity of adenyl cyclase to stimulation by noradrenaline (b) no response in tissue levels of cyclic AMP when stimulated by isoprenaline and (c) impaired release of glycerol following stimulation with isoprenaline. The other child, with similar clinical features, showed abnormal deposits of glycogen in the liver. It is postulated that a primary metabolic defect occurs in peripheral adipose tissue (and possibly at other sites such as the liver) that interferes with triglyceride (and glycogen) mobilization during prolonged malnutrition.
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PMID:Triglyceride storage disease. A report of two affected children associated with neurological abnormalities. 18 5

Cholera toxin may depress cell-mediated immunity by stimulation of adenyl cyclase and production of cyclic AMP in cellular systems or when given parenterally to experimental animals. Whether or not similar effects might be found during clinical infection with Vibrio cholerae was the subject of this study. Delayed hypersensitivity reactions to skin test antigens were found to be markedly depressed in Bengali patients with cholera 24 h after fluid repletion. Skin test response rates were lower in children and in adults with the disease than in both normal adults and children or in adults with an equivalent degree of malnutrition. Patients with equal degrees of dehydration due to noncholera diarrhea were significantly less immunosuppressed. Concurrent depression of other manifestations of cell-mediated immunity was not found.
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PMID:Depression of cell-mediated immunity in cholera. 42 32

The reported incidence of "pathogenic" bacteria, as judged by serotype, in the stools of children with acute diarrhoea has varied from 4 to 33% over the last twenty years. Techniques such as tissue culture provide a means for detecting enterotoxin-producing strains of bacteria, strains which often do not possess "pathogenic" serotypes. "Pathogenicity" requires redefinition, and the aetiological importance of bacteria in diarrhoea is probably considerably greater than previous reports have indicated. Colonization of the bowel by a pathogen will result in structural and/or mucosal abnormalities, and will depend on a series of complex interactions between the external environment, the pathogen, and the host and its resident bacterial flora. Enteropathogenic bacteria may be broadly classified as (i) invasive (e.g. Shigella, Salmonella and some Escherichia coli) which predominantly affect the distal bowel, or (ii) non-invasive (e.g. Vibrio cholerae and E. coli) which affect the proximal bowel. V. cholerae and E. coli elaborate heat-labile enterotoxins which activate adenylate cyclase and induce small intestinal secretion; the secretory effects of heat-stable E. coli and heat-labile Shigella dysenteriae enterotoxins are not accompanied by cyclase activation. The two major complications of acute diarrhoea are (i) hypernatraemic dehydration with its attendant neurological, renal and vascular lesions, and (ii) protracted diarrhoea which may lead to severe malnutrition. Deconjugation of bile salts and colonization of the small bowel with toxigenic strains of E. coli may be important in the pathophysiology of the protracted diarrhoea syndrome. The control of bacterial diarrhoea requires a corrdinated political, educational, social, public health and scientific attack. Bacterial diarrhoea is a major health problem throughout the world, and carries an appreciable morbidity and mortality. This is particularly the case during infancy, and in those developing parts of the world where malnutrition is common. This paper is concerned mainly with acute bacterial diarrhoea, and reviews the problem as a whole.
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PMID:The problem of bacterial diarrhoea. 79 97

Homeostasis of the internal environment in mammals is accomplished by a series of feedback mechanisms in a variety of tissues. Homeostasis of cell structure and function during marked changes in the environment is equally important. Both types of homeostasis are dependent on adjustments in endocrine function and changes in enzyme activity. In some instances the intracellular servomechanisms required for homeostasis match in vigor and range the perturbations of the external environment. The regulation of cell metabolism is accomplished by enzymatic, membranous and genetic mechanisms. Most peptide hormones act by combining with a specific receptor in the membrane of sensitive cells, which activates adenyl cyclase to produce cyclic AMP which in turn has selective second messenger functions. Insulin and somatotropin appear to be exceptions and may act via cyclic GMP. Steroid hormones, on the other hand, pass through the cell membrane and combine with a specific receptor protein in the cytoplasm of sensitive cells. This receptor then serves as a transport system for movement of the hormone to the nucleus where it stimulates specific protein synthesis. Nutritional effects on enzyme synthesis are partially direct and partially mediated by the endocrine system. Trace nutrients, especially the fat-soluble vitamins, appear to act directly to modify specific protein syntheses, whereas the bulkier constituents of the diet (carbohydrate, fat protein) exert their effects principally through altered rates of secretion of insulin, glucagon, and the glucocortioids. Protein-calorie malnutrition is the result of a massive assault on homeostatic and adaptive mechanisms designed to conserve nutrients and preserve life. The pathogenesis of marasmus and kwashiorkor is discussed in the light of these adaptive mechanisms.
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PMID:Introductory remarks: nutrient, hormone, enzyme interactions. 80 21

The purpose of this study was to evaluate the coupled beta-adrenergic receptor (BAR) and adenylate cyclase (AC) system of the lung during the course of the bleomycin-(Bleo) induced pulmonary fibrosis in hamsters. The BAR population, dissociation constants (Kd), AC activity, and its sensitivity to various stimulators were studied at 2, 4, 7, 14, and 21 days after intratracheal administration of either 1 unit of Bleo or an equivalent volume of saline. The BAR population in the lungs of Bleo-treated animals did not differ from control at the early times, but it was significantly reduced to 5.9 X 10(3) fmol and 3.6 X 10(3) fmol from the control values of 1.1 X 10(4) fmol and 1.5 X 10(4) fmol per lung at 14 and 21 days after treatment, respectively. The Kd values for control hamster lung ranged from 2.5 X 10(-11) M to 3.7 X 10(-11) M, and for Bleo-treated hamster lung, from 2.7 X 10(-11) M to 4.8 X 10(-11) M. The Kd at the earliest time, 2 days after treatment, did not differ significantly from the Kd values at the subsequent times in control, while for Bleo-treated hamster lung, the Kd values at 7, 14, and 21 days were significantly higher than the Kd at 2 days after treatment. The Kd values for Bleo-treated hamster lung were also significantly higher than control at 14 and 21 days. The AC activity of the lung in Bleo-treated hamster was significantly reduced to 67%, 40%, 38%, and 50% of their respective controls in response to H2O (basal), GTP (10(-4) M), GTP + isoproterenol (10(-4) M each), and NaF (10 mM) at 21 days after treatment. The extent of AC stimulation in Bleo-treated hamster lung in response to various stimulators was generally less than that of saline control. Reductions in the BAR population and increased Kd values in Bleo-treated hamster lung were attributed to its fibrogenic ability and not to nutritional deficiency, which may partly be accountable for decreased AC activity of the lung in these animals. However, there were qualitative differences in the lung AC activity between Bleo-treated and nutritionally deprived hamsters, since the enzyme from the latter group was generally more responsive to stimulators than the enzyme from the former group. It was concluded from the findings of this study that an impairment in the coupled BAR and AC system of the lung may be partly responsible for the fibrogenic ability of bleomycin.
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PMID:Impairment in coupled beta-adrenergic receptor and adenylate cyclase system during bleomycin-induced lung fibrosis in hamsters. 245 79

Malnutrition, as well as malignancy, induces alterations in heart metabolism and performance. Previous studies have implicated adrenergic mechanisms as the cause. The present study was undertaken to investigate if the adenylate cyclase system in the rat heart was affected by malnutrition. Three different animal groups with malnutrition were compared with a control group: rats with acute starvation for 14-96 hours, rats with protein-calorie malnutrition for 2 weeks, and rats with tumors. Stimulation by beta-adrenergic receptors and inhibition by muscarinic receptors of adenylate cyclase activity were not altered by malnutrition. However, conditions used for in vitro adenylate cyclase determinations were, of necessity, not physiological. Neither did the number of beta-adrenergic and muscarinic receptors change. When competition-binding experiments were performed, differences comprising agonist affinity and affinity state distribution were noted among the groups. The myocardial beta-adrenergic receptors formed a reduced number of high-affinity sites in all groups as compared with the control rats. All high-affinity sites displayed a more than 10-fold increase in affinity toward isoproterenol and an impaired sensitivity to guanine nucleotides except in heart membranes derived from rats starved less than 48 hours. While the protein-calorie restricted and the tumor-bearing rats had myocardial beta-adrenergic receptors that were unresponsive to guanine nucleotides, after 48 hours of starvation the rats exhibited an attenuated guanine-nucleotide-induced affinity shift. No changes associated with malnutrition in myocardial membrane levels of the of the stimulatory guanine-nucleotide-binding protein were detected by cholera-toxin-induced ADP-ribosylation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of malnutrition on rat myocardial beta-adrenergic and muscarinic receptors. 253 24

Acute neonatal malnutrition alters lumenal glycoproteins as demonstrated by altered lectin binding. To determine the effect of a 72-h fast on lumenal glycolipids, specifically the monosialoganglioside GM1, we quantitated cholera toxin (CT) binding and adenylate cyclase activity. The calculated number of specific sites for CT binding to microvillus membrane (MVM) from newborn rabbits fasted for 72 h was decreased in MVM from proximal small bowel (7 +/- 0.8 x 10(8)/micrograms protein) compared to 72-h control neonatal rabbits (18 +/- 3.3 x 10(8) micrograms protein). In distal small bowel there was no difference in the calculated receptor sites/micrograms MVM protein between fasted (8 +/- 1.7 x 10(8)) and fed (11 +/- 4 x 10(8)) groups. MVM prepared from proximal small bowel of fed animals bound significantly more CT than MVM prepared from distal small bowel of fed animals. The affinity for CT was the same in all MVM preparations. Neuraminidase treatment of MVM resulted in increased CT binding in fed and fasted rabbit proximal and distal MVM preparations, but the greatest increase occurred in MVM prepared from proximal small bowel from fasted animals. There was no difference in adenylate cyclase activity in fed, fasted, and proximal or distal small bowel crude membrane preparations. Refeeding (120 h) resulted in normalization of CT binding in MVM from proximal small bowel of fasted animals. We conclude a 72-h fast in neonatal rabbits resulted in decreased regional CT binding in MVM prepared from proximal small bowel of fasted animals, but no change in adenylate cyclase activity. Refeeding reverses CT binding abnormalities.
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PMID:Short term neonatal starvation altered cholera toxin binding in rabbits. 291 2

We evaluated the effects of a hyperosmolar lactose load on the functional properties of the jejunal mucosa of protein-energy malnourished rats. Malnourished animals exposed to an oral lactose load showed an enhanced loss of DNA, protein, and sodium into the intestinal lumen as compared to well nourished controls exposed to the same lactose load. Only the jejunum of lactose-fed malnourished rats showed increased levels of 3'-5' cyclic adenosine monophosphate (cAMP), that appeared principally due to an enhancement of adenyl cyclase. Overall, our data strongly suggest that the intestinal mucosa in malnutrition is more sensitive and responds to an osmotic stress by enhanced secretion.
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PMID:Cyclic AMP-mediated jejunal secretion in lactose-fed malnourished rats. 298 27

The stimulation of intestinal adenylate cyclase by cholera toxin (CT) was studied in normal and malnourished rats 4 to 24 hr after a 30-min incubation of intestinal loops with the toxin. Whereas in control rats the enzyme activity returned to basal levels after 12 hr of incubation, in malnourished rats the activity of the enzyme remained significantly elevated even after 24 hr of the initial incubation. Malnourished animals had a reduced turnover rate of intestinal cells as determined by thymidine kinase activity. The delayed turnover of intoxicated cells may account for continuous activation of mucosal adenylate cyclase and possibly for prolongation of diarrhea in malnutrition.
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PMID:Stimulation of intestinal adenylate cyclase by cholera toxin in malnourished rats. 393 Oct 85

The metabolism of adenosine 3',5'-monophosphate (cyclic AMP) was studied in specific pathogen-free mice exposed to neonatal infection with mouse enterovirus or to malnutrition during early life. Metabolic activity was determined by measuring the turnover of cyclic AMP-8-(14)C to respiratory (14)CO(2), its incorporation into various organs and plasma, and the binding activity of synaptosome for cyclic AMP. Early malnutrition increased the catabolism of cyclic AMP as measured by expiration in respiratory CO(2). The level of cyclic AMP was lower in plasma and its incorporation into various tissues was decreased in infected and malnourished animals. Metabolic products of cyclic AMP were isolated from plasma by ion exchange chromatography. Cyclic AMP-8-(14)C had completely disappeared 9 hr after injection. Fewer metabolites of cyclic AMP were detected in infected or malnourished groups than in controls and the metabolic reaction from 5'-AMP to adenosine seemed to be slow in these animals. The ability to incorporate cyclic AMP to synaptosome was also impaired in the experimental groups. The concentrations of brain cyclic AMP were lower in infected or malnourished animals than in controls. Depression of accumulation of cyclic AMP probably resulted from excessive activity of phosphodiesterase, rather than from impairment of adenyl cyclase. Intraperitoneal administration of theophylline brought the activity level of phosphodiesterase to normal in infected or malnourished mice; this fact probably accounted for enhanced accumulation of brain cyclic AMP.
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PMID:Lasting biological effects of early environmental influences. VII. Metabolism of adenosine in mice exposed to early environmental stress. 433 97


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