THREE-STEP-REGULATION OF ACID-BASE BALANCE IN BODY FLUID AFTER ACID LOAD

Renal mechanisms for the maintenance of acid-base balance were studied in the normal bullfrog, during metabolic and respiratory acidosis, and after carbonic anhydrase inhibition. Following intravenous administration of 0.3–12 mmole HCl/ kg, as 0.1 n HCl, urinary pH (initially pH 6.3–7.7) did not change significantly. However, urinary ammonia excretion increased more than twofold, and within 3–5 days the cumulative increase was equivalent to the acid load given. Despite the increased ammonia excretion, chloride excretion did not increase after acid loading. In both normal and acidotic bullfrogs ammonia excretion was correlated with an increase in urinary pH. Respiratory acidosis in the small frog, Rana limnocharis, produced by exposure to 6.4% CO2 in air, induced neither urinary acidification nor increased ammonia excretion; both urinary sodium and bicarbonate excretion increased. When renal carbonic anhydrase was inhibited by acetazoleamide injection, urine flow, sodium excretion, and bicarbonate excretion increased markedly, urinary pH increased slightly, and urinary ammonia excretion remained unchanged. These renal responses to acidosis are compared with those of the acidotic dog.

Download Full-text

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

Nutrients ◽

10.3390/nu11081913 ◽

2019 ◽

Vol 11 (8) ◽

pp. 1913 ◽

Cited By ~ 4

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.

Download Full-text

Is urea formation regulated primarily by acid-base balance in vivo?

AJP Renal Physiology ◽

10.1152/ajprenal.1986.250.4.f605 ◽

1986 ◽

Vol 250 (4) ◽

pp. F605-F612 ◽

Cited By ~ 2

Author(s):

M. L. Halperin ◽

C. B. Chen ◽

S. Cheema-Dhadli ◽

M. L. West ◽

R. L. Jungas

Keyword(s):

Dietary Protein ◽

Urea Synthesis ◽

Acid Base Balance ◽

Severe Metabolic Acidosis ◽

Acid Base ◽

Wide Range ◽

Base Balance ◽

Acid Load ◽

Acid Base Status

Large quantities of ammonium and bicarbonate are produced each day from the metabolism of dietary protein. It has recently been proposed that urea synthesis is regulated by the need to remove this large load of bicarbonate. The purpose of these experiments was to test whether the primary function of ureagenesis in vivo is to remove ammonium or bicarbonate. The first series of rats were given a constant acid load as hydrochloric acid or ammonium chloride; individual rats received a constant nitrogen load at a time when their plasma acid-base status ranged from normal (pH 7.4, 28 mM HCO3) to severe metabolic acidosis (pH 6.9, 6 mM HCO3). Urea plus ammonium excretions and the blood urea, glutamine, and ammonium concentrations were monitored with time. Within the constraints of non-steady-state conditions, the rate of urea synthesis was constant and the plasma glutamine and ammonium concentrations also remained constant; thus it appears that the rate of urea synthesis was not primarily regulated by the acid-base status of the animal in vivo over a wide range of plasma ammonium concentrations. In quantitative terms, the vast bulk of the ammonium load was converted to urea over 80 min; only a small quantity of ammonium appeared as circulating glutamine or urinary ammonium. Urea synthesis was proportional to the nitrogen load. A second series of rats received sodium bicarbonate; urea synthesis was not augmented by a bicarbonate load. We conclude from these studies that the need to dispose of excess bicarbonate does not primarily determine the rate of ureagenesis in vivo. The data support the classical view that ureagenesis is controlled by the quantity of ammonium to be removed.

Download Full-text

Effects of protein, methionine, or chloride on acid-base balance and on cysteine catabolism

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1995.269.5.e910 ◽

1995 ◽

Vol 269 (5) ◽

pp. E910-E917 ◽

Cited By ~ 3

Author(s):

D. L. Bella ◽

M. H. Stipanuk

Keyword(s):

Adaptive Response ◽

Sulfur Amino Acids ◽

Acid Base Balance ◽

Acid Base ◽

Low Protein ◽

Metabolic Compensation ◽

Base Balance ◽

Acid Load ◽

Excess Sulfur ◽

Intact Rats

Metabolism of cysteine to sulfate results in production of H+, whereas metabolism of cysteine to taurine does not. Rats were fed a basal low-protein diet or a diet with excess protein, methionine, or chloride for 2-3 wk, and effects of these treatments on acid-base homeostasis and on cysteine metabolism were determined. Hepatocytes from rats fed diets with excess methionine, but not from rats fed diets with excess protein or chloride, catabolized a high proportion of cysteine to taurine (32% vs. 4-7% for other groups), and intact rats fed excess methionine excreted more sulfur as taurine (51% of total sulfur vs. 1-6% for other groups). The formation of taurine vs. sulfate as the end product of cysteine catabolism provides a metabolic compensation that minimizes the acid load in rats fed excess sulfur amino acids. However, increased production of taurine vs. sulfate is not a general adaptive response to acidogenic diets.

Download Full-text

Food Composition and Acid-Base Balance: Alimentary Alkali Depletion and Acid Load in Herbivores

Journal of Nutrition ◽

10.1093/jn/138.2.431s ◽

2008 ◽

Vol 138 (2) ◽

pp. 431S-434S ◽

Cited By ~ 4

Author(s):

Heidrun Kiwull-Schöne ◽

Peter Kiwull ◽

Friedrich Manz ◽

Hermann Kalhoff

Keyword(s):

Food Composition ◽

Acid Base Balance ◽

Acid Base ◽

Base Balance ◽

Acid Load

Download Full-text

U-Shaped Association between Dietary Acid Load and Risk of Osteoporotic Fractures in 2 Populations at High Cardiovascular Risk

Journal of Nutrition ◽

10.1093/jn/nxaa335 ◽

2020 ◽

Vol 151 (1) ◽

pp. 152-161

Author(s):

Jesús Francisco García-Gavilán ◽

Alfredo Martínez ◽

Jadwiga Konieczna ◽

Rafael Mico-Perez ◽

Ana García-Arellano ◽

...

Keyword(s):

Cardiovascular Risk ◽

Osteoporotic Fractures ◽

Heart Association ◽

Acid Base Balance ◽

High Cardiovascular Risk ◽

Acid Base ◽

Base Balance ◽

Dietary Acid ◽

Acid Load ◽

Predimed Study

ABSTRACT Background Bone contributes to maintaining the acid-base balance as a buffering system for blood pH. Diet composition also affects acid-base balance. Several studies have linked an imbalance in the acid-base system to changes in the density and structure of bone mass, although some prospective studies and meta-analyses suggest that acid load has no deleterious effect on bone. Objective The aim of this study was to examine the associations between potential renal acid load (PRAL) and net endogenous acid production (NEAP) and the risk of osteoporotic fractures and bone mineral density (BMD) in 2 middle-aged and elderly Mediterranean populations. Methods We conducted a longitudinal analysis including 870 participants from the PREvención con DIeta MEDiterranea (PREDIMED) Study and a cross-sectional analysis including 1134 participants from the PREDIMED-Plus study. Participants were adults, aged 55–80 y, either at high cardiovascular risk (PREDIMED) or overweight/obese with metabolic syndrome (PREDIMED-Plus), as defined by the International Diabetes Federation, the American Heart Association, and the National Heart Association. PRAL and NEAP were calculated from validated food-frequency questionnaires. BMD was measured using DXA scans. Fracture information was obtained from medical records. The association between mean PRAL and NEAP and fracture risk was assessed using multivariable-adjusted Cox models. BMD differences between tertiles of baseline PRAL and NEAP were evaluated by means of ANCOVA. Results A total 114 new fracture events were documented in the PREDIMED study after a mean of 5.2 y of intervention and 8.9 y of total follow-up. Participants in the first and third PRAL and NEAP tertiles had a higher risk of osteoporotic fracture compared with the second tertile, showing a characteristically U-shaped association [HR (95% CI): 1.73 (1.03, 2.91) in tertile 1 and 1.91 (1.14, 3.19) in tertile 3 for PRAL, and 1.83 (1.08, 3.09) in tertile 1 and 1.87 (1.10, 3.17) in tertile 3 for NEAP]. Compared with the participants in tertile 1, the participants in the top PRAL and NEAP tertiles had lower BMD [PRAL: mean total femur BMD: 1.029 ± 0.007 and 1.007 ± 0.007 g/cm2; P = 0.006 (tertiles 1 and 3); NEAP: mean total femur BMD: 1.032 ± 0.007 and 1.009 ± 0.007 g/cm2; P = 0.017 (tertiles 1 and 3)]. Conclusions The results of our study suggest that both high and low dietary acid are associated with a higher risk of osteoporotic fractures, although only high dietary acid was found to have a negative relation to BMD in senior adults with existing chronic health conditions. This trial was registered at http://www.isrctn.com/ as ISRCTN3573963 (PREDIMED) and ISRCTN89898870 (PREDIMED-Plus).

Download Full-text