Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At 0-3 days of age the plasma ammonium concentration in full term appropriate for gestational age (AGA) infants was (mean +/- SEM) 27.5 +/- 0.5 micron; a value similar to that reported in adults. Ammonium levels in low birthweight AGA and SGA groups were 47.0 +/- 2.0 micron and 45.1 +/- 3.3 micron respectively; significantly elevated (P less than 0.001) as compared to the full term group. These increased ammonium levels persisted at 3-5 weeks of age. Associated with the hyperammonemia was a significant (P less than 0.01) decrease in plasma alpha-ketoglutarate concentration: 11.8 +/- 1.0 micron, in the low birthweight AGA as compared to 20.7 +/- 0.6 micron in the full term AGA infants. There was an inverse linear correlation between plasma concentrations of ammonium and alpha-ketoglutarate r = -0.86, P less than 0.001. Urinary orotate excretion was significantly elevated (P less than 0.05) in low birthweight AGA infants. There was no difference in the plasma concentrations of glutamine, glutamate, or alanine among the various groups. Hyperammonemia was not associated with neurologic dysfunction.
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PMID:Asymptomatic hyperammonemia in low birthweight infants. 64 93

To delineate the potential role of disordered glucose and glucose-precursor kinetics in the abnormal carbohydrate metabolism of chronic renal failure, alanine and glucose production and utilization and gluconeogenesis from alanine were studied in patients with chronic compensated renal insufficiency and in normal volunteers. With simultaneous primed injection-continuous infusions of radiolabeled alanine and glucose, rates of metabolite turnover and precursor-product interrelationships were calculated from the plateau portion of the appropriate specific activity curves. All subjects were studied in the postabsorption state. In 13 patients with chronic renal failure (creatinine = 10.7+/-1.2 mg/100 ml; mean+/-SEM), glucose turnover was found to be 1,035+/-99.3 mumol/min. This rate was increased 56% (P = 0.003) over that observed in control subjects (664+/-33.5 mumol/min). Alanine turnover was 474+/-96.0 mumol/min in azotemic patients. This rate was 191% greater (P = 0.007) than the rate determined in control subjects (163+/-19.4 mumol/min). Gluconeogenesis from alanine and the percent of glucose production contributed by gluconeogenesis from alanine were increased in patients with chronic renal failure (192% and 169%, respectively) as compared to controls (P < 0.05 for each). Alanine utilization for gluconeogenesis was increased from 40.2+/-3.86 mumol/min in control subjects to 143+/-39.0 mumol/min in azotemic patients (P < 0.05). The percent of alanine utilization accounted for by gluconeogenesis was not altered in chronic renal insufficiency. In nondiabetic azotemic subjects, mean fasting glucose and immunoreactive insulin levels were increased 24.3% (P = 0.005) and 130% (P = 0.046), respectively.These results in patients with chronic renal failure demonstrate (a) increased glucose production and utilization, (b) increased gluconeogenesis from alanine, (c) increased alanine production and utilization, and (d) a relative impairment to glucose disposal. We conclude that chronic azotemia is characterized by increased rates of glucose and glucose precursor flux and by a relative impairment to glucose disposal. These findings may suggest an underlying hepatic and peripheral insensitivity to the metabolic action of insulin in patients with chronic renal insufficiency.
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PMID:Abnormal carbohydrate metabolism in chronic renal failure. The potential role of accelerated glucose production, increased gluconeogenesis, and impaired glucose disposal. 65 34

An angiotensin II (A II) analogue (1-Sar-8-Ala-angiotensin II) (saralasin) was infused into 418 untreated hypertensive subjects during a 1-day evaluation while blood pressure was recorded every 2 minutes by Arteriosonade. At 5 mug/kg per min, saralasin produced a change in mean blood pressure which correlated significantly (r=-0.54, P less than 0.001) with the stimulated plasma renin activity (PRA) (after intravenous furosemide and ambulation for 2 hours. Saralasin caused a rise inmean blood pressure of at least 7.0 mm Hg in 97 hypertensive subjects, who also had a low stimulated PRA (1.3+/-SEM, 0.1 ng/ml per hour; normal range, 1.7-8.5). On a low sodium diet, the pressor response of hypertensive subjects to saralasin continued and was an even better indicator of a low stimulated PRA. Infusion of saralasin at 10 mug/kg per min into normal subjects on an unrestricted diet, a low sodium diet, and a high sodium diet produced, respectively, no change, a fall (P less than 0.05), and a rise (P less than 0.005) in blood pressure. The same saralasin dose in six hypertensive subjects who showed a pressor response to the analogue in the 1-day study also produced a rise in blood pressure when given on a low sodium diet, and this rise was more than twice that seen in normal subjects on a high sodium diet. Hypertensive subjects who showed the pressor response had a significantly greater (P less than 0.01) pressor sensitivity to A II than did hypertensive nonresponders to saralasin and noraml subjects on an uncontrolled diet. The affinity of the vascular receptors for the analogue was greater in the hypertensive group that showed the pressor response to saralasin. In summary, the pressor response to saralasin, as defined above, occurred in 23% of a large unselected group of hypertensive subjects and was associated with salt loading, a low stimulated PRA, and increased pressor sensitivity to A II.
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PMID:Pressor response to 1-sar-8-ala-angiotensin II (saralasin) in hypertensive subjects. 83 71

1. Administration of dexamethasone, 8 mg/day (0-02 mmol/day), for 5 days to normal subjects produced negative nitrogen balance, due to early and sustained increases in urinary urea nitrogen excretion 2. In eight subjects ingesting 0-9--1-6 g of protein day-1 kg-1 body weight the cumulative increment in urea nitrogen excretion averaged + 12-5 g (SEM 2-8, P less than 0-01) over the 5 days of glucocorticoid administration. 3. Increases in urinary urea nitrogen excretion could be related to both plasma alanine and blood glutamine changes by using a multiple regression equation. 4. These results suggest that corticosteroids induce increased release of alanine and glutamine by peripheral tissues, which may augment urea formation and negative nitrogen balance. 5. The correlation between increments in urea nitrogen excretion and increases in plasma arginine remains unexplained.
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PMID:The role of alanine and glutamine in steroid-induced nitrogen wasting in man. 91 44

Cellophane perinephritis hypertension was produced in four dogs, while five additional dogs served as normotensive controls. A competitive antagonist of angiotensin II, 1-sarcosine-8-alanine angiotensin II, was infused iv into these conscious dogs at a rate of 6 mug/min/kg of body weight for 45 min. Arterial pressure averaged 170 +/- 11 (SEM) mm Hg in the dogs with perinephritic hypertension, and was not altered significantly during infusion of the angiotensin antagonist. In the normal dogs the arterial pressure averaged 100 +/- 10 mm Hg and likewise, did not change during administration of the angiotensin analog. Plasma renin activity values were essentially the same in these two groups of dogs and did not change during infusion of the angiotensin antagonist. These studies provide strong evidence that the renin-angiotensin system is not involved in maintaining the elevated arterial pressure in dogs with chronic hypertension produced by cellophane perinephritis.
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PMID:Role of the renin-angiotensin system in dogs with perinephritis hypertension. 96 86

Plasma glucose, glucagon, and insulin responses to oral feedings of L-alanine were assessed in 44 healthy term infants during the first three days of life. Alanine administration produced significant increases in glucagon and glucose concentrations on day 1, but not on days 2 and 3. These increases occurred within 30 minutes (mean and SEM for glucagon, 127 plus or minus 7 to 219 plus or minus 16 pg/ml, P smaller than 0.001; glucose, 45 plus or minus 3 to 60 plus or minus 7 mg/100 ml, P smaller than 0.01) and persisted at the P smaller than 0.05 level at four hours. Responsiveness to alanine seemed to be related to the baseline blood glucose levels since constant infusions of glucose inhibited the response; These results indicate that the pancreatic islet alpha cell secretion mechanism(s) is functioning in the newborn.
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PMID:The effect of oral alanine on blood glucose and glucagon in the human newborn infant. 116 64

1. 31P n.m.r. spectroscopy in vivo was used to study the effect of L-alanine infusion on the concentrations of gluconeogenic intermediates in normal human liver. Studies were performed in six healthy male subjects (34-44 years, fasted overnight) using a chemical shift imaging pulse sequence on a whole-body n.m.r. system operating at 1.6T. Hepatic 31P n.m.r. spectra were obtained from 10 min before to 70 min after intravenous administration of 0.70 (n = 2), 1.40 (n = 3) or 2.80 (n = 5) nmol of L-alanine/kg body weight over 4.5 min. Concentrations of phosphomonoesters, Pi and phosphodiesters relative to ATP were calculated from peak areas in the n.m.r. spectra, using the beta-ATP peak as a reference. 2. Dose-dependent spectral changes were observed for [phosphomonoesters]/[ATP] and [Pi]/[ATP]. At the highest dose given, maximal changes in [phosphomonoesters]/[ATP] (mean +/- SEM: 98 +/- 12%, P < 0.005) and [Pi]/[ATP] (-33 +/- 3%, P < 0.001) were observed approximately 45 min after the L-alanine infusion. [Phosphodiesters]/[ATP] showed a maximal increase of 24 +/- 6% (P < 0.05), which was independent of the L-alanine dose. Hepatic ATP levels and pH did not change. 3. To identify the metabolites responsible for the changes observed in vivo, male Wistar rats were infused with 11.2 mmol of L-alanine/kg body weight. After 15 min, livers were freeze-clamped and were extracted according to standard procedures. In vitro, 31P n.m.r. spectra obtained at 8.4 or 11.7 T revealed sharp increases in the concentrations of 3-phosphoglycerate and phosphoenolpyruvate after L-alanine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of L-alanine infusion on 31P nuclear magnetic resonance spectra of normal human liver: towards biochemical pathology in vivo. 132 34

To investigate the effect of substrates during oral rehydration therapy, we studied intestinal cation cotransport (ICC) with glutamine (Gln), alanine (Ala) and glucose (Glu). The specific aims were to determine the biological effects of these three different cotransport systems on intestinal function. Isolated rabbit ileal mucosa preparations mounted in Ussing chambers were studied. ICC was determined by measuring short-circuit current (Isc) and potential difference (PD) while monitoring tissue resistance (TR). The data are reported as the mean +/- SEM of 4-6 experiments for each amino acid concentration. Increasing concentrations of Gln (10(-5) to 10(-2) M), Ala (10(-5) to 10(-1) M) and Glu (10(-5) to 10(-2) M) caused a significant (P < 0.05) increase in ICC. Gln (30 mM) and Ala (0.1 M) had a maximal effect (Em(Gln) = 100% and Em(Ala) = 66%, P < 0.05) which was higher than that obtained with 30 mM Glu (Em(Glu) = 35%). When sodium was replaced with choline on the mucosal side, Ringer solution completely abolished the response with Gln, Ala and Glu. The presence of all three substrates (10(-2) M Gln, 10(-1) M Ala, and 10(-2) M Glu) in Ringer solution on the mucosal side caused a significant increase in ICC (delta increase of short circuit current = 111 +/- 43 microA, P < 0.05). These results demonstrate that Gln, Ala and Glu each increased sodium-dependent cation cotransport, and that sodium-dependent intestinal cation cotransport was higher with Gln than with Ala or Glu.
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PMID:Cotransport of sodium with glutamine, alanine and glucose in the isolated rabbit ileal mucosa. 134 39

Cerebrospinal fluid (CSF) from 20 male patients with nonneurologic disease (age 64.5 +/- 2.8 SEM) was analyzed for the presence of the serpin alpha 1-antichymotrypsin (alpha 1-ACT). A chymotrypsin-specific chromogenic substrate (succinyl-Ala-Ala-Pro-Phe-p-nitroanilide) was used to examine the CSF samples. All CSF samples showed inhibitory activity ranging from 45 to 80% inhibition. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of the samples revealed the presence of a 68-kDa protein migrating identical to authentic human plasma alpha 1-ACT. Complex formation was performed with iodinated bovine chymotrypsin for several representative CSF samples having the highest chymotrypsin inhibitory activity. Comparison was made with complex formation performed with commercially available authentic human plasma alpha 1-ACT. These studies showed the formation of complexes at 37 degrees C, regardless of whether the sample was subsequently boiled or not. In the case of CSF, two complex bands, mass smaller than with plasma alpha 1-ACT, were formed at the lower temperature whereas a single higher Mr band was formed when the samples were boiled. To determine whether cleavage of the serpin occurred, these studies were repeated using human neutrophil cathepsin G as target protease. A complex of approximately 90 kDa was formed with human alpha 1-ACT under these same conditions. alpha 1-ACT has been detected in senile amyloid plaques in brains of Alzheimer's disease patients, the only plasma serine protease inhibitor localized to these structures. Another serpin, protease nexin I, is also found in these plaques, but this inhibitor does not circulate in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of the serpin, alpha 1-antichymotrypsin, in normal human cerebrospinal fluid. 172 48

The development of a new technique to investigate maternal-fetal transfer across the near term guinea-pig yolk sac placenta by in-situ perfusion of the yolk sac vessels is described. The maternal-fetal transfer of labeled water, D- and L-glucose, O-methyl-D-glucose (oMDG), D- and L-alanine, D- and L-aspartate, L-lactate and alpha-amino-isobutyric acid (AIBA) was investigated after injection of these substances into the maternal circulation. After 15 min of perfusion at 0.5 ml/min the water clearance was 132 +/- 12 microliters/min (SEM, n = 30). The clearances for D- or L-glucose were less than 1.2 microliters/min. The activity of label in the venous yolk sac perfusate of all other substances was not different from background activity when 14C-label was used. The clearance of 3H-L-alanine approached the clearance value of water. The total uptake (as defined for single-injection double tracer dilution experiments) from the perfusate of D-glucose, oMDG, alanine and aspartate in comparison to L-glucose was also studied. Mean D-glucose uptake was 11.2 +/- 1.9 percent (n = 8), it was significantly reduced to 4.9 +/- 2 percent (n = 5) by cytochalasin B (1 X 10(-4) mmol/l), and by increasing concentrations of D-glucose (1 to 20 mmol/l, n = 4). The uptake of oMDG was 8.8 +/- 1.5 percent (n = 8). L-alanine uptake was 25 +/- 3.4 percent, D-alanine uptake was 8.3 +/- 1.5 percent (n = 12). Both uptake values were decreased significantly by 10 mmol/l L-alanine, but unaffected by [Na+] (less than 15 mequ/l). There was no uptake of AIBA. The uptakes of L-aspartate were 34.9 +/- 3.7 percent and of D-aspartate 40.4 +/- 4.8 percent (n = 11). Both uptake values were significantly and reversibly reduced by 1 mmol/l L-aspartate and D-aspartate, and by low [Na+] (less than 15 mequ/l). It is concluded that water can move by diffusion from maternal circulation into the yolk sac capillaries in considerable amounts whereas the contribution of the yolk sac placenta to fetal nutrition with D-glucose, L-alanine and L-aspartate is negligible. The membranes of yolk sac cells contain specific transport systems for D-glucose, D-/L-alanine and D-/L-aspartate transfer. The function of the vitelline placenta in the near-term guinea-pig is comparable more to the gut than to the chorio-allantoic placenta.
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PMID:The artificially perfused guinea-pig yolk sac placenta: transfer and uptake of water, glucose and amino acids. 177 43


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