scholarly journals The effect of metabolic acidosis on the synthesis and turnover of rat renal phosphate-dependent glutaminase

1986 ◽  
Vol 233 (1) ◽  
pp. 139-144 ◽  
Author(s):  
J Tong ◽  
G Harrison ◽  
N P Curthoys
Keyword(s):  
Metabolic Acidosis ◽  
Total Protein ◽  
Rat Kidney ◽  
Relative Rate ◽  
Normal Animal ◽  
Acid Base Balance ◽  
Acid Base ◽  
A Value ◽  
Base Balance ◽  
Glutaminase Activity

Regulation of the mitochondrial phosphate-dependent glutaminase activity is an essential component in the control of renal ammoniagenesis. Alterations in acid-base balance significantly affect the amount of the glutaminase that is present in rat kidney, but not in brain or small intestine. The relative rates of glutaminase synthesis were determined by comparing the amount of [35S]methionine incorporated into specific immunoprecipitates with that incorporated into total protein. In a normal animal, the rate of glutaminase synthesis constitutes 0.04% of the total protein synthesis. After 7 days of metabolic acidosis, the renal glutaminase activity is increased to a value that is 5-fold greater than normal. During onset of acidosis, the relative rate of synthesis increases more rapidly than the appearance of increased glutaminase activity. The increased rate of synthesis reaches a plateau within 5 days at a value that is 5.3-fold greater than normal. Recovery from chronic acidosis causes a rapid decrease in the relative rate of glutaminase synthesis, but a gradual decrease in glutaminase activity. The former returns to normal within 2 days, whereas the latter requires 11 days. The apparent half-time for glutaminase degradation was found to be 5.1 days and 4.7 days for normal and acidotic rats respectively. These results indicate that the increase in renal glutaminase activity associated with metabolic acidosis is due primarily to an increase in its rate of synthesis. From the decrease in activity that occurs upon recovery from acidosis, the true half-life for the glutaminase was estimated to be 3 days.

Chronic metabolic acidosis upregulates rat kidney Na-HCO 3 − cotransporters NBCn1 and NBC3 but not NBC1

2002 ◽  
Vol 282 (2) ◽  
pp. F341-F351 ◽  
Author(s):  
Tae-Hwan Kwon ◽  
Christiaan Fulton ◽  
Weidong Wang ◽  
Ira Kurtz ◽  
Jørgen Frøkiær ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Rat Kidney ◽  
Free Access ◽  
Thick Ascending Limb ◽  
Acid Base Balance ◽  
Acid Base ◽  
Chronic Metabolic Acidosis ◽  
Daily Water Intake ◽  
Base Balance ◽  
Access To Water

Several members of the Na-HCO[Formula: see text] cotransporter (NBC) family have recently been identified functionally and partly characterized, including rkNBC1, NBCn1, and NBC3. Regulation of these NBCs may play a role in the maintenance of intracellular pH and in the regulation of renal acid-base balance. However, it is unknown whether the expressions of these NBCs are regulated in response to changes in acid-base status. We therefore tested whether chronic metabolic acidosis (CMA) affects the abundance of these NBCs in kidneys using two conventional protocols. In protocol 1, rats were treated with NH4Cl in their drinking water (12 ± 1 mmol · rat−1 · day−1) for 2 wk with free access to water ( n = 8). Semiquantitative immunoblotting demonstrated that whole kidney abundance of NBCn1 and NBC3 in rats with CMA was dramatically increased to 995 ± 87 and 224 ± 35%, respectively, of control levels ( P < 0.05), whereas whole kidney rkNBC1 was unchanged (88 ± 14%). In protocol 2, rats were given NH4Cl in their food (10 ± 1 mmol · rat−1 · day−1) for 7 days, with a fixed daily water intake ( n = 6). Consistent with protocol 1, whole kidney abundances of NBCn1 (262 ± 42%) and NBC3 (160 ± 31%) were significantly increased compared with controls ( n = 6), whereas whole kidney rkNBC1 was unchanged (84 ± 17%). In both protocols, immunocytochemistry confirmed upregulation of NBCn1 and NBC3 with no change in the segmental distribution along the nephron. Consistent with the increase in NBCn1, measurements of pH transients in medullary thick ascending limb (mTAL) cells in kidney slices revealed two- to threefold increases in DIDS- sensitive, Na+-dependent HCO[Formula: see text] uptake in rats with CMA. In conclusion, CMA is associated with a marked increase in the abundance of NBCn1 in the mTAL and NBC3 in intercalated cells, whereas the abundance of NBC1 in the proximal tubule was not altered. The increased abundance of NBCn1 may play a role in the reabsorption of NH[Formula: see text] in the mTAL and increased NBC3 in reabsorbing HCO[Formula: see text].

Renal ammonium production—une vue canadienne

1987 ◽  
Vol 65 (4) ◽  
pp. 489-498 ◽  
Author(s):  
J. T. Brosnan ◽  
M. Lowry ◽  
P. Vinay ◽  
A. Gougoux ◽  
M. L. Halperin
Keyword(s):  
Metabolic Acidosis ◽  
Glutamine Metabolism ◽  
Ammonium Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Ammonium Production ◽  
Alternate Fuels ◽  
Glutaminase Activity ◽  
Stimulation Of

The purpose of this review is to examine the factors regulating ammonium production in the kidney and to place these factors in the perspective of acid–base balance. Renal ammonium production and excretion are required to maintain acid–base balance. However, only a portion of renal ammonium production is specifically stimulated by metabolic acidosis. One should examine urinary ammonium excretion at three levels: distribution of ammonium between blood and urine, augmented glutamine metabolism, and an energy constraint due to ATP balance considerations. With respect to the biochemical regulation of acid–base renal ammonium production, an acute stimulation of α-ketoglutarate dehydrogenase by a fall in pH seems to be important but this may not be the entire story. In chronic metabolic acidosis augmented glutamine entry into mitochondria (dog) or increased phosphate-dependent glutaminase activity (rat) become critical to support a high flux rate. Metabolic alterations, which diminish the rate of oxidation of alternate fuels, might also be important. The above principles are discussed in the ketoacidosis of fasting, the clinically important situation of high rates of renal ammonium production.

scholarly journals ASSOCIATION OF ACID-BASE PARAMETERS WITH LACTATE LEVEL IN CRITICALLY ILL PATIENTS WITH METABOLIC ACIDOSIS

2018 ◽  
Vol 24 (2) ◽  
pp. 141
Author(s):  
Donaliazarti Donaliazarti ◽  
Rismawati Yaswir ◽  
Hanifah Maani ◽  
Efrida Efrida
Keyword(s):  
Metabolic Acidosis ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Lactate Level ◽  
Linear Regression Analysis ◽  
P Value ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Parameters ◽  
Base Balance

Metabolic acidosis is prevalent among critically ill patients and the common cause of metabolic acidosis in ICU is lactic acidosis. However, not all ICUs can provide lactate measurement. The traditional method that uses Henderson-Hasselbach equation (completed with BE and AG) and alternative method consisting of Stewart and its modification (BDEgap and SIG), are acid-base balance parameters commonly used by clinicians to determine metabolic acidosis in critically ill patients. The objective of this study was to discover the association between acid-base parameters (BE, AGobserved, AGcalculated, SIG, BDEgap) with lactate level in critically ill patients with metabolic acidosis. This was an analytical study with a cross-sectional design. Eighty-four critically ill patients hospitalized in the ICU department Dr. M. Djamil Padang Hospital were recruited in this study from January to September 2016. Blood gas analysis and lactate measurement were performed by potentiometric and amperometric method while electrolytes and albumin measurement were done by ISE and colorimetric method (BCG). Linear regression analysis was used to evaluate the association between acid-base parameters with lactate level based on p-value less than 0.05. Fourty five (54%) were females and thirty-nine (46%) were males with participant’s ages ranged from 18 to 81 years old. Postoperative was the most reason for ICU admission (88%). Linear regression analysis showed that p-value for BE, AGobserved, AGcalculated, SIG and BDEgap were 119; 0.967; 0.001; 0.001; 0.689, respectively. Acid-base balance parameters which were mostly associated with lactate level in critically ill patients with metabolic acidosis were AGcalculated and SIG. 

Effect of systemic acid-base balance on ileal secretion

1987 ◽  
Vol 253 (3) ◽  
pp. G330-G335
Author(s):  
D. S. Goldfarb ◽  
P. M. Ingrassia ◽  
A. N. Charney
Keyword(s):  
Metabolic Acidosis ◽  
Cholera Toxin ◽  
Metabolic Disorders ◽  
Respiratory Acidosis ◽  
Secretory Process ◽  
Sprague Dawley ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Change ◽  
Base Balance

We previously reported that systemic pH and HCO3 concentration affect ileal water and electrolyte absorption. To determine whether these effects could influence an ongoing secretory process, we measured transport in ileal loops exposed to either saline or 50-75 micrograms cholera toxin in mechanically ventilated Sprague-Dawley rats anesthetized with pentobarbital sodium. The effects of acute respiratory and metabolic acidosis and alkalosis were then examined. Decreases in systemic pH during respiratory acidosis caused equivalent increases in net water (54 +/- 8 microliters . cm-1 . h-1) and Na absorption (7 +/- 1 mu eq . cm- . h-1) and smaller increases in Cl absorption in cholera toxin compared with saline loops. These increases reversed the net secretion of these ions observed during alkalemia in the cholera toxin loops to net absorption. Metabolic acidosis and alkalosis and respiratory compensation of systemic pH of these metabolic disorders also altered cholera toxin-induced secretion in a direction consistent with the pH change. The increase in net HCO3 secretion caused by cholera toxin was unaffected by the respiratory disorders and did not vary with the HCO3 concentration in the metabolic disorders. These findings suggest that the systemic acid-base disorders that characterize intestinal secretory states may themselves alter intestinal absorptive function and fluid losses.

Basic Interpretation of Metabolic Acidosis

2010 ◽  
Vol 30 (5) ◽  
pp. 63-69 ◽  
Author(s):  
Melissa Beaudet Jones
Keyword(s):  
Metabolic Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Common Causes ◽  
Base Balance ◽  
The Common ◽  
Basic Concepts

What are the basic concepts of acid-base balance, the 2 types of metabolic acidosis, and the common causes of each type of metabolic acidosis?

scholarly journals A role for bicarbonate in the regulation of mammalian glutamine metabolism

1979 ◽  
Vol 184 (3) ◽  
pp. 599-606 ◽  
Author(s):  
G Baverel ◽  
P Lund
Keyword(s):  
Rat Kidney ◽  
Glutamine Metabolism ◽  
Kidney Cortex ◽  
Complete Oxidation ◽  
Kidney Tubules ◽  
Acid Base Balance ◽  
Acid Base ◽  
Rat Kidney Cortex ◽  
Base Balance

1. The concentration of HCO3- (independent of any change of pH) exerts different effects on glutamine metabolism in rat kidney-cortex tubules, hepatocytes and enterocytes.2. In kidney tubules HCO3- (10.5-50 MM) has no effect on glutaminase (EC 3.5.1.2), whereas glutamate dehydrogenase (EC 1.4.1.3) is inhibited as HCO3- concentration is increased. The result is that flux through the entire glutamate-to-glucose pathway is inhibited by increasing HCO3- concentrations. A large proportion (more than 30%) of the glutamine removed undergoes complete oxidation. 3. In hepatocytes, and to a smaller extent in enterocytes, HCO3- is an accelerator of glutaminase. Synthesis of glucose and urea from glutamine in hepatocytes increases as HCO3- concentration is increased. Calculations show that fumarate, formed via aspartate aminotransferase and arginino-succinate lyase, is the precursor of the glucose. There is no complete oxidation of the carbon skeleton of glutamine in hepatocytes. 4. Leucine at near-physiological concentrations (0.1-1 mM) is an accelerator of glutaminase in hepatocytes, but not in kidney tubules or in enterocytes. 5. The results are discussed in relation to regulation of acid/base balance in vivo.

scholarly journals Associations between Dietary Acid Load and Biomarkers of Inflammation and Hyperglycemia in Breast Cancer Survivors

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1913 ◽  
Author(s):  
Tianying Wu ◽  
Phoebe Seaver ◽  
Hector Lemus ◽  
Kathryn Hollenbach ◽  
Emily Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metabolic Acidosis ◽  
Cancer Survivors ◽  
Breast Cancer Survivors ◽  
Acid Base Balance ◽  
Acid Base ◽  
Dietary Acid Load ◽  
Base Balance ◽  
Dietary Acid ◽  
Acid Load

Metabolic acidosis can lead to inflammation, tissue damage, and cancer metastasis. Dietary acid load contributes to metabolic acidosis if endogenous acid–base balance is not properly regulated. Breast cancer survivors have reduced capacities to adjust their acid–base balance; yet, the associations between dietary acid load and inflammation and hyperglycemia have not been examined among them. We analyzed data collected from 3042 breast cancer survivors enrolled in the Women’s Healthy Eating and Living (WHEL) Study who had provided detailed dietary intakes and measurements of plasma C-reactive protein (CRP) and hemoglobin A1c (HbA1c). Using a cross-sectional design, we found positive associations between dietary acid load and plasma CRP and HbA1c. In the multivariable-adjusted models, compared to women with the lowest quartile, the intakes of dietary acid load among women with the highest quartile showed 30–33% increases of CRP and 6–9% increases of HbA1c. Our study is the first to demonstrate positive associations between dietary acid load and CRP and HbA1c in breast cancer survivors. Our study identifies a novel dietary factor that may lead to inflammation and hyperglycemia, both of which are strong risk factors for breast cancer recurrence and comorbidities.

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