Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Human gastrointestinal secretions formed soluble copper complexes when labelled in vitro with 64Cu. 2. Copper-binding substances of low molecular weight were demonstrated in the saliva, gastric juice and secretin-stimulated duodenal aspirate of nomal subjects by dialysis and gel-chromatography studies. 3. The nature of the copper complexes formed by secretions obtained from patients with Wilson's disease was similar to that oc complexes formed by secretions of normal subjects. 4. Bile contained a copper-binding fraction of high molecular weight which was more concentrated in gall-bladder than hepatic bile. Between pH 5 and pH 8, this component had a greater binding affinity EDTA at a concentration of 10 mmol/1. 5. Absorption of 64Cu from 64Cu-labelled saliva, gastric juice or L-histidine solution (100 mmol/1) administered intraduodenally into groups of rats was similar to that observed in a control series given [Cu]cupric acetate in sodium chloride solution. In contrast, the absorption of 64Cu from labelled hepatic and gall-bladder bile was significantly reduced. 6. The results suggest that dietary copper forms soluble complexes with the alimentary secretions and that these complexes influence absorption of the metal according to their molecular size. The net uptake of ingested copper from the gut lumen ms, low-molecular-weight ligands in the alimentary secretions and a macromolecular copper-binding complex of bile.
Clin Sci Mol Med 1975 Sep
PMID:Studies on the nature of complexes formed by copper with human alimentary secretions and their influence on copper absorption in the rat. 24 May 30

The synthesis of the transport systems (enzymeII-complexes) coded for in the mtl and in the gut (srl) operon was found to be induced by unphosphorylated D-mannitol and D-glucitol respectively. Induction from the outside however is only possible if these polyols are taken up into the cells. Induction of the D-mannitol system is immediate, resistant against catabolite repression, relatively insensitive towards transient repression and starts from a high uninduced level (5--30%). By contrast, the induction of the D-glucitol system starts at a low basal level (0.5--2.5%), does show a pronounced lag from 25 to 90 min, and is hypersensitive towards catabolite and transient repression. These differences apparently reflect primarely differences in the corresponding operator-promotor genes mtl (P,O) and gut (P,O) as well as differences in the uptake of the first, inducing hexitol molecules. For each operon additional regulatory genes exist, called mtlR and gutR respectively, in which transrecessive, temperature sensitive mutations leading to a constitutive expression of the corresponding operon can be found. The influence of these regulatory mechanisms in diauxie experiments and their importance for the differentiation of the three operons during evolution from apparently one common ancestor operon will be discussed.
Mol Gen Genet 1978 Aug 17
PMID:Analysis of the regulatory mechanisms controlling the synthesis of the hexitol transport systems in Escherichia coli K12. 36 44

The transport systems (enzymeII-complexes of the PEP-dependent sugar:phosphotransferase system) coded for in the mtl and in the gut (srl) operon of E. coli K12 have been shown to be the pacemaker enzymes in the catabolism of the two hexitols D-mannitol and D-glucitol, respectively. As for other pacemaker enzymes their activity is regulated in a complex way: (i) via competitive inhibition by analogues. (ii) via non-competitive (feedback) inhibition by the simultaneous, rapid uptake of a number of structurally related or non-related carbohydrates, regardless if these are transported by group translocation, active transport or facilitated diffusion. This type of inhibition is strongly reinforced, if the inhibitory carbohydrates are converted efficiently into hexose-phosphates at the same time. Among these, predominantly D-fructose-6-P seems to act as a feedback inhibitor for the hexitol specific enzymeII-complexes: (iii) inhibition of hixitol-phosphate accumulation by D-glucose-6-P. The influence of additional parameters (PEP level, P approximately HPr level) and indications for the existence of further mechanisms controlling the activity of hexitol and other carbohydrate transport systems will be discussed, as will be the part the inhibitory mechanisms described above play in the phenomena of transient repression and inducer exclusion.
Mol Gen Genet 1978 Nov 16
PMID:Analysis of regulatory mechanisms controlling the activity of the hexitol transport systems in Escherichia coli K12. 36 87

1. We have measured the incorporation of an intraperitoneal injection of [3H] glutamate into the protein of the gut, liver and kidney of lean and obese siblings of the genetically obese mouse. 2. Recycling of the 3H was minimized by using glutamate labelled at the C-2 position. Loss of label from the amino acid pool by transamination and deamination was rapid, with a half-life of 4 h. 3. In tissue protein the amino acid showing the highest 3H radioactivity was glutamate. 4. The half-lives for protein synthesis and catabolism were calculated from the decay curves of both specific and total radioactivity of [3H] glutamate in tissue protein. No significant differences were found between kidney, liver and gut in lean and obese mice.
Clin Sci Mol Med 1978 Apr
PMID:A new technique for measuring protein turnover in the gut, liver and kidneys of lean and obese mice with [3H] glutamic acid. 63 74

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a 'functional immaturity' of the pancreas.
Clin Sci Mol Med 1976 Mar
PMID:Glucose tolerance and insulin release in malnourished rats. 81 69

1. A whole-gut perfusion technique has been used to compare the rates of intestinal absorption of sodium and xenon. 2. The calculated transit-time spectra for sodium and xenon across the gut mucosa do not differ significantly either in mean transit time or, for the first 15 min, in shape. 3. These results support the hypothesis that the rate of transfer of sodium from the small intestinal lumen to plasma is limited by blood flow. 4. It is suggested that some features of cholera can be explained by the hypothesis.
Clin Sci Mol Med 1977 Mar
PMID:The relative transfer rates for sodium and xenon from gut lumen to plasma in man. 84 55

The number of ribosomal RNA cistrons has been measured in the total DNA extracted from L2 juvenile and adult stages of the free-living nematode Panagrellus silusiae. Saturation hybridization studies with homologous rRNA indicate that both stages have about 275 ribosomal genes per haploid equivalent. Using homologous 125I-labelled rRNA for in situ hybridization, the mean number of silver grains per DNA content for oocyte, hypodermis and gut nuclei was similar. The mean DNA contents of maturing oocyte, hypodermis and gut nuclei are about 20C, 2C, and 10C respectively. We conclude that rDNA amplication alone is insufficient to account for the variation in DNA content of oocytes and that postembryonic development in this eutelic organism occurs without a significant differential increase in the number of ribosomal cistrons per worm.
Mol Gen Genet 1976 Sep 23
PMID:Relative ribosomal RNA cistron multiplicity in oocytes and postembryonic stages of the eutelic nematode Panagrellus silusiae. 98 26

1. The roles of the kidney and the small intestine in the conjugation of bromosulphthalein have been compared with that of the liver. 2. Studies with homogenates indicated that the liver has a higher bromosulphthalein-glutathione-conjugating activity than the intestine and kidney. The reduced glutathione content of the liver is greater than that of the small intestine and kidneys, which contain comparable amounts. 3. Experiments in vitro with tissue slices confirmed that the three organ are able to extract significant amount of bromosulphthalein. In carbon tetrachloride-induced hepatic necrosis the uptake and conjugation of the dye by the liver were reduced but were increased in the kidney and unchanged in the small intestine. 4. After an intravenous injection of bromosulphthalein, the percentages conjugated in the liver, kidney and gut were similar.
Clin Sci Mol Med 1976 Dec
PMID:The role of small intestine and kidney in bromosulphthalein conjugation. 107 Apr 24

1. The relation between endogenous urea metabolism and albumin synthesis has been studied in ten patients with chronic renal failure and in four normal subjects, after single intravenous injections of [14-C]urea,[15-N]urea and 125-I-labelled albumin. 2. The rate of urea synthesis was determined from the dynamics of plasma [14-C]urea specific radioactivity and the rate of urea metabolism was estimated from the relative rates of urea synthesis and urea appearance in urine and body water. Deconvolution analysis of plasma [15N]albumin enrichmevt and 125-i-labelled albumin radioactivity yielded the cumulative incorporation of 15-N into total exchangeable albumin and enabled calculation of the absolute rate of urema nitrogen utilization for albumin synthesis. 3. Although the mean absolute rate of urea degradation in uraemic patients (3-7 mmol/h) was higher than in normal subjects (2-3 mmol/h) there was no significant positive correlation between urea degradation and plasma urea concentration. 4. In uraemic subjects, there was a significant positive correlation between urea synthetic rate and urea degration rate. 5. The rate of utilization of urea nitrogen for albumin synthesis was low, but was very much higher in uraemic subjects (mean 83-8 mumol/h) compared with normal subjects (mean 6-4 mumol/h), as was the provision by urea of the nitrogen required for albumin synthesis in uraemic subjects (2-37%) compared with normal subjects (0-13%). 6. The efficiency of utilization of urea nitrogen for albumin synthesis was higher in the uraemic patients (1-3%) than the normal subjects (0-2%), and was higher in those patients with chronic renal failure who received a 30 g protein diet than those on 70 g of protein. A significant negative correlation was noted between efficiency of urea nitrogen utilization and the rate of synthesis of albumin. 7. These studies suggest the presence of a mechanism for the conservation of urea nitrogen in chronic renal failure which is unrelated to the extent of urea degradation, and which can only be partly explained by the higher proportion of intraluminal gut nitrogen derived from urea.
Clin Sci Mol Med 1975 May
PMID:Efficiency of utilization of urea nitrogen for albumin synthesis by chronically uraemic and normal man. 112 30

1. Rabbits in balance on a low sodium diet were given doses of sodium chloride either orally or intravenously. 2. Those receiving oral doses responded with a much greater natriuresis than those receiving intravenous ones. 3. This could be explained by the existence of a sodium input monitor somewhere in the gut or portal circulation.
Clin Sci Mol Med 1975 Nov
PMID:A comparison on natriuresis after oral and intravenous sodium loading in sodium-depleted rabbits: evidence for a gastrointestinal or portal monitor of sodium intake. 119


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