Glutamine Production Rate and its Contribution to Urinary Ammonia in Normal Man

1982 ◽  
Vol 62 (3) ◽  
pp. 299-305 ◽  
Author(s):  
M. H. N. Golden ◽  
P. Jahoor ◽  
A. A. Jackson

1. Glutamine [15N]amide was infused at a steady rate of 33.34 μmol/h into seven male adult volunteers who were in the fed state and normal acid-base status. 2. Plasma glutamine amide N enrichment and urinary ammonia N enrichment rose to a constant value within 3 h. 3. The glutamine production rate was 51.8 ± 7.9 mmol/h. 4. The total ammonia excretion rate was 0.87 mmol/h. Of this excreted ammonia 62.6 ± 9% was derived from the amide N atom of glutamine. 5. The excreted glutamine amide N (0.53 mmol/h) was only 1% of the glutamine production. If half the ammonia formed by the kidney is excreted in urine and half liberated into the renal vein in subjects with normal acid-base status [E. E. Owen & R. R. Robinson (1963) Journal of Clinical Investigation, 42, 263–276], then the kidney accounts for only 2% of glutamine disposal. 6. Whole body protein turnover, measured from the urinary [15N]ammonia enrichment, was 30.3 ± 7.7 g of N/day (2.8 g of protein day−1 kg−1).

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shuangyao Wang ◽  
Chris G. Carter ◽  
Quinn P. Fitzgibbon ◽  
Basseer M. Codabaccus ◽  
Gregory G. Smith

AbstractThis is the first study in an aquatic ectotherm to combine a stoichiometric bioenergetic approach with an endpoint stochastic model to explore dietary macronutrient content. The combination of measuring respiratory gas (O2 and CO2) exchange, nitrogenous (ammonia and urea) excretion, specific dynamic action (SDA), metabolic energy substrate use, and whole-body protein synthesis in spiny lobster, Sagmariasus verreauxi, was examined in relation to dietary protein. Three isoenergetic feeds were formulated with varying crude protein: 40%, 50% and 60%, corresponding to CP40, CP50 and CP60 treatments, respectively. Total CO2 and ammonia excretion, SDA magnitude and coefficient, and protein synthesis in the CP60 treatment were higher compared to the CP40 treatment. These differences demonstrate dietary protein influences post-prandial energy metabolism. Metabolic use of each major energy substrate varied at different post-prandial times, indicating suitable amounts of high-quality protein with major non-protein energy-yielding nutrients, lipid and carbohydrate, are critical for lobsters. The average contribution of protein oxidation was lowest in the CP50 treatment, suggesting mechanisms underlying the most efficient retention of dietary protein and suitable dietary inclusion. This study advances understanding of how deficient and surplus dietary protein affects energy metabolism and provides approaches for fine-scale feed evaluation to support sustainable aquaculture.


1986 ◽  
Vol 123 (1) ◽  
pp. 93-121 ◽  
Author(s):  
C. L. Milligan ◽  
C. M. Wood

Exhaustive exercise induced a severe short-lived (0–1 h) respiratory, and longer-lived (0–4 h) metabolic, acidosis in the extracellular fluid of the rainbow trout. Blood ‘lactate’ load exceeded blood ‘metabolic acid’ load from 1–12 h after exercise. Over-compensation occurred, so that by 8–12 h, metabolic alkalosis prevailed, but by 24 h, resting acid-base status had been restored. Acid-base changes were similar, and lactate levels identical, in arterial and venous blood. However, at rest venous RBC pHi was significantly higher than arterial (7.42 versus 7.31). After exercise, arterial RBC pHi remained constant, whereas venous RBC pHi fell significantly (to 7.18) but was fully restored by 1 h. Resting mean whole-body pHi, measured by DMO distribution, averaged approx. 7.25 at a pHe of approx. 7.82 and fell after exercise to a low of 6.78 at a pHe of approx. 7.30. Whole-body pHi was slower to recover than pHe, requiring up to 12 h, with no subsequent alkalosis. Whole-body ECFV decreased by about 70 ml kg-1 due to a fluid shift into the ICF. Net H+ excretion to the water increased 1 h after exercise accompanied by an elevation in ammonia efflux. At 8–12 h, H+ excretion was reduced to resting levels and at 12–24 h, a net H+ uptake occurred. Lactate excretion amounted to approx. 1% of the net H+ excretion and only approx. 2% of the whole blood load. Only a small amount of the anaerobically produced H+ in the ICF appeared in the ECF and subsequently in the water. By 24 h, all the H+ excreted had been taken back up, thus correcting the extracellular alkalosis. The bulk of the H+ load remained intracellular, to be cleared by aerobic metabolism.


2021 ◽  
Vol 320 (1) ◽  
pp. R55-R68
Author(s):  
Alex M. Zimmer ◽  
Milica Mandic ◽  
Hong Meng Yew ◽  
Emma Kunert ◽  
Yihang K. Pan ◽  
...  

In fishes, branchial cytosolic carbonic anhydrase (CA) plays an important role in ion and acid-base regulation. The Ca17a isoform in zebrafish ( Danio rerio) is expressed abundantly in Na+-absorbing/H+-secreting H+-ATPase-rich (HR) cells. The present study aimed to identify the role of Ca17a in ion and acid-base regulation across life stages using CRISPR/Cas9 gene editing. However, in preliminary experiments, we established that ca17a knockout is lethal with ca17a−/− mutants exhibiting a significant decrease in survival beginning at ∼12 days postfertilization (dpf) and with no individuals surviving past 19 dpf. Based on these findings, we hypothesized that ca17a−/− mutants would display alterations in ion and acid-base balance and that these physiological disturbances might underlie their early demise. Na+ uptake rates were significantly increased by up to 300% in homozygous mutants compared with wild-type individuals at 4 and 9 dpf; however, whole body Na+ content remained constant. While Cl− uptake was significantly reduced in ca17a−/− mutants, Cl− content was unaffected. Reduction of CA activity by Ca17a morpholino knockdown or ethoxzolamide treatments similarly reduced Cl− uptake, implicating Ca17a in the mechanism of Cl− uptake by larval zebrafish. H+ secretion, O2 consumption, CO2 excretion, and ammonia excretion were generally unaltered in ca17a−/− mutants. In conclusion, while the loss of Ca17a caused marked changes in ion uptake rates, providing strong evidence for a Ca17a-dependent Cl− uptake mechanism, the underlying causes of the lethality of this mutation in zebrafish remain unclear.


2001 ◽  
Vol 184 (7) ◽  
pp. 1422-1426 ◽  
Author(s):  
Sean C. Blackwell ◽  
Julie Moldenhauer ◽  
Sonia S. Hassan ◽  
Mark E. Redman ◽  
Jerrie S. Refuerzo ◽  
...  

1998 ◽  
Vol 95 (3) ◽  
pp. 339 ◽  
Author(s):  
Bernadette A.C. VAN ACKER ◽  
Karel W.E. HULSEWÉ ◽  
Anton J.M. WAGENMAKERS ◽  
Nicolaas E.P. DEUTZ ◽  
Bernard K. VAN KREEL ◽  
...  

2018 ◽  
Vol 65 ◽  
pp. 429-448
Author(s):  
D. Joe Millward

John Waterlow was an inspiring clinical and laboratory-based nutritional scientist, who was recognized as paterfamilias of a large, international and influential group of distinguished acolytes. His early work was characterized by study of the nature and clinical management of infantile malnutrition, notably as director of the MRC's Tropical Metabolism Research Unit, which he established in Jamaica in 1954. His London period, from 1970 until and beyond his official retirement in 1982, involved him as Head of the Nutrition Department at the London School of Hygiene & Tropical Medicine. Here he established a Clinical Nutrition and Metabolism Unit to continue his experimental animal and human studies researching protein metabolism; he also assumed the role of the the UK's most influential public health nutritionist, becoming President of the Nutrition Society. Like all great scientists, his work encompassed a very wide range of scientific disciplines, although he modestly described himself as a physiologist, consistent with his primary Cambridge training. Above all, throughout his career, he was happiest as an experimentalist at the bench, from his first assignment studying heat stroke of British troops in the Iraq desert during the Second World War to his measurement of [ 15 N] enrichment in urea as part of his study of whole-body protein turnover just prior to his retirement, working with an isotope ratio mass spectrometer which, like much of the equipment he used, he had largely assembled himself.


2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Javier Enrique Cely ◽  
Oscar G. Rocha ◽  
María J. Vargas ◽  
Rafael M. Sanabria ◽  
Leyder Corzo ◽  
...  

Background. Acid-base disorders have been previously described in patients with chronic hemodialysis, with metabolic acidosis being the most important of them; however, little is known about the potential changes in acid-base status of patients on dialysis living at high altitudes. Methods. Cross-sectional study including 93 patients receiving chronic hemodialysis on alternate days and living in Bogotá, Colombia, at an elevation of 2,640 meters (8,661 feet) over sea level (m.o.s.l.). Measurements of pH, PaCO2, HCO3, PO2, and base excess were made on blood samples taken from the arteriovenous fistula (AVF) during the pre- and postdialysis periods in the midweek hemodialysis session. Normal values for the altitude of Bogotá were taken into consideration for the interpretation of the arterial blood gases. Results. 43% (n= 40) of patients showed predialysis normal acid-base status. The most common acid-base disorder in predialysis period was metabolic alkalosis with chronic hydrogen ion deficiency in 19,3% (n=18). Only 9,7% (n=9) had predialysis metabolic acidosis. When comparing pre- and postdialysis blood gas analysis, higher postdialysis levels of pH (7,41 versus 7,50, p<0,01), bicarbonate (21,7mmol/L versus 25,4mmol/L, p<0,01), and base excess (-2,8 versus 2,4, p<0,01) were reported, with lower levels of partial pressure of carbon dioxide (34,9 mmHg versus 32,5 mmHg, p<0,01). Conclusion. At an elevation of 2,640 m.o.s.l., a large percentage of patients are in normal acid-base status prior to the dialysis session (“predialysis period”). Metabolic alkalosis is more common than metabolic acidosis in the predialysis period when compared to previous studies. Paradoxically, despite postdialysis metabolic alkalosis, PaCO2 levels are lower than those found in the predialysis period.


1976 ◽  
Vol 50 (3) ◽  
pp. 185-194 ◽  
Author(s):  
J. Yudkin ◽  
R. D. Cohen

1. The isolated perfused kidneys of fed rats in normal acid-base status showed a constant rate of lactate removal from the perfusate between 5 and 90 min of perfusion at a perfusate pH of 7·4–7·5. 2. Lactate removal by kidneys of rats in normal acid-base status was stimulated within 30 min by a reduction in perfusate pH to 7·1–7·2, but depressed when perfusate pH was reduced further. 3. Kidneys taken from rats previously made acidotic and perfused with media of various pH values showed a progressive fall in the rate of lactate removal during the perfusion. 4. Glucose output by the kidneys of rats in normal acid—base status perfused with lactate as substrate was not affected by an alteration in perfusate pH. The kidneys of acidotic rats generally showed an increased rate of glucose output compared with those of control rats.


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