scholarly journals Glutamine synthetase activity of muscle in acidosis

1983 ◽  
Vol 216 (2) ◽  
pp. 523-525 ◽  
Author(s):  
P A King ◽  
L Goldstein ◽  
E A Newsholme
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Acidosis ◽  
Glutamine Synthetase ◽  
Maximum Activity ◽  
Synthetase Activity ◽  
Glutamine Synthetase Activity ◽  
Adrenal Steroids ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Metabolic acidosis stimulates the rate of glutamine release from muscle, and this in turn is used by the kidney in acid-base balance. NH4Cl, HCl or diabetic ketoacidosis increases the maximum activity of glutamine synthetase in skeletal muscle. Starvation and administration of adrenal steroids also increase the activity of the enzyme in muscle.

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.

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].

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?

Alterations in glutamine synthetase activity in rat skeletal muscle are associated with advanced age

Nutrition ◽  
2006 ◽  
Vol 22 (7-8) ◽  
pp. 778-785 ◽  
Author(s):  
Carole Pinel ◽  
Véronique Coxam ◽  
Michelle Mignon ◽  
Daniel Taillandier ◽  
Christine Cubizolles ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glutamine Synthetase ◽  
Advanced Age ◽  
Synthetase Activity ◽  
Glutamine Synthetase Activity ◽  
Rat Skeletal Muscle

Effects of potassium and rubidium on muscle cell bicarbonate

1962 ◽  
Vol 203 (1) ◽  
pp. 209-214 ◽  
Author(s):  
James B. Hudson ◽  
Arnold S. Relman
Keyword(s):  
Skeletal Muscle ◽  
Intraperitoneal Injection ◽  
Renal Cortex ◽  
Acid Base Balance ◽  
Acid Base ◽  
Sharp Rise ◽  
Extracellular Acidosis ◽  
Rapid Exchange ◽  
Base Balance ◽  
K Depletion

A tissue CO2 content method was used to study the effects of Rb and K on skeletal muscle bicarbonate and pH in rats. Intraperitoneal injection of large loads of RbCl or KCl in normal rats produced extracellular acidosis and a transient intracellular alkalosis in muscle (and also in renal cortex). This supports previous suggestions that rapid exchange of administered cation for intracellular hydrogen occurs. In K-deficient alkalotic rats, loading with RbCl or KCl caused a greater fall in extracellular bicarbonate but a smaller rise in muscle bicarbonate. Muscle bicarbonate was unchanged by the alkalosis of K depletion or the reduction in extracellular bicarbonate resulting from chronic feeding of Rb. After the acute RbCl and KCl loads, repair of intracellular alkalosis occurred within 6 hr, associated with a transient sharp rise in tissue citrate content. It is suggested that production of citrate and other metabolic acids may play a role in stabilizing cellular acid-base balance.

Enzymes of glutamine metabolism in inflammation associated with skeletal muscle hypertrophy

1989 ◽  
Vol 257 (6) ◽  
pp. E885-E894 ◽  
Author(s):  
T. B. Kelso ◽  
C. R. Shear ◽  
S. R. Max
Keyword(s):  
Skeletal Muscle ◽  
Connective Tissue ◽  
Glutamine Synthetase ◽  
Pentose Phosphate Pathway ◽  
Tissue Repair ◽  
Time Course ◽  
Pentose Phosphate ◽  
Synthetase Activity ◽  
Glutamine Synthetase Activity ◽  
Plantaris Muscle

Glutamine synthesis and utilization were studied in the plantaris muscle after removal of its functional synergists, the soleus and gastrocnemius muscles. Rat plantaris muscle was compared with unoperated controls at 7, 14, and 30 days after synergist ablation and induction of hypertrophy. Glutamine synthetase activity increased from 6.17 +/- 1.77 to 33.92 +/- 2.23 nmol.h-1.mg protein-1, and glutaminase activities increased from 98.63 +/- 23.05 to 478.70 +/- 64.17 nmol.h-1.mg protein-1 7 days after surgery and remained elevated at 14 and 30 days. Sham-operated controls examined 7 days after surgery did not exhibit significantly increased glutamine synthetase activity. Histological examination revealed a large proliferation of connective tissue cells, as well as cells involved in tissue repair and inflammation; this influx was maximal 1 wk after surgery. The activity of the oxidative enzymes of the pentose phosphate pathway increased from 3.08 +/- 4.31 to 20.86 +/- 1.13 nmol.min-1.mg protein-1 1 wk after surgery. The time course of changes in pentose phosphate pathway enzymes was similar to that of the increases in glutamine synthetase, glutaminase, and cellular infiltration. Increases in muscle wet weight followed a different time course than changes in glutamine synthetase, glutaminase, and pentose phosphate pathway activities. It is concluded that the initial increases in plantaris muscle weight are probably due to edema, connective tissue proliferation, and cells involved in tissue repair and inflammation. The increase in glutamine synthetase activity appears to occur in skeletal muscle, whereas the changes in glutaminase and pentose phosphate pathway activities appear to represent infiltrating inflammatory cells. Furthermore, the increase in glutamine synthetase activity may serve to support the infiltrating cells, which appear to lack substantial capacity for glutamine production. These results represent a functional relationship between skeletal muscle glutamine synthesis and utilization by cells mediating inflammation and connective tissue repair and synthesis.

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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