Effects of dietary protein-load and alkaline supplementation on acid–base balance and glucose metabolism in healthy elderly

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.

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Dietary protein influences acid-base balance in sedentary horses

Journal of Equine Veterinary Science ◽

10.1016/j.jevs.2005.09.006 ◽

2005 ◽

Vol 25 (10) ◽

pp. 434-438 ◽

Cited By ~ 4

Author(s):

Patricia M. Graham-Thiers ◽

David S. Kronfeld

Keyword(s):

Dietary Protein ◽

Acid Base Balance ◽

Acid Base ◽

Base Balance

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Effects of Moderate Hypoxemia and Unilateral Carotid Ligation on Cerebral Glucose Metabolism and Acid-Base Balance in the Rat

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1989.52 ◽

1989 ◽

Vol 9 (3) ◽

pp. 342-349 ◽

Cited By ~ 8

Author(s):

Alan H. Lockwood ◽

Kathryn E. Peek ◽

Masahiro Izumiyama ◽

Eddy W. H. Yap ◽

Jocelyn Labove

Keyword(s):

Glucose Metabolism ◽

Clinical Symptoms ◽

Brain Slices ◽

Acid Base Balance ◽

Acid Base ◽

Caudate Putamen ◽

Tissue Ph ◽

Carotid Ligation ◽

Base Balance ◽

Medial Geniculate

We used our recently developed method for the simultaneous measurement of the local CMRglc (LCMRglc) and composite tissue pH to evaluate the response to unilateral carotid ligation and moderate hypoxia [40.1 ± 4.8 (SD) mm Hg]. The LCMRglc and tissue pH were measured simultaneously in brain slices using [14C]2-deoxy-d-glucose and [14C]5,5-dimethyl-2,4-oxazolidinedione. The ipsilateral LCMRglc was increased significantly in the caudate-putamen and medial thalamus and was surrounded by a much more extensive zone of acidosis, as shown by significant reductions in the tissue pH, which was affected in parietal cortex, caudate-putamen, lateral septal nucleus, medial geniculate, Ammon's horn, and nucleus reticularis of substantia nigra. In regions with an elevated LCMRglc and acidosis, anaerobic glycolysis combined with ATP hydrolysis are likely to co-exist. In regions characterized by normal glucose metabolism and acidosis, we hypothesize that a direct effect of hypoxia on the sodium/hydrogen ion antiporter may lead to secondary acidosis. Disturbed acid-base balance during hypoxia may have an adverse effect on cerebral function and cause clinical symptoms.

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Higher Dietary Acidity is Associated with Lower Bone Mineral Density in Postmenopausal Iranian Women, Independent of Dietary Calcium Intake

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000207 ◽

2014 ◽

Vol 84 (3-4) ◽

pp. 0206-0217 ◽

Cited By ~ 8

Author(s):

Seyedeh-Elaheh Shariati-Bafghi ◽

Elaheh Nosrat-Mirshekarlou ◽

Mohsen Karamati ◽

Bahram Rashidkhani

Keyword(s):

Calcium Intake ◽

Dietary Calcium ◽

Dietary Calcium Intake ◽

Dietary Intakes ◽

Iranian Women ◽

Acid Base Balance ◽

Mineral Density ◽

Acid Base ◽

Base Balance ◽

Dietary Acid

Findings of studies on the link between dietary acid-base balance and bone mass are relatively mixed. We examined the association between dietary acid-base balance and bone mineral density (BMD) in a sample of Iranian women, hypothesizing that a higher dietary acidity would be inversely associated with BMD, even when dietary calcium intake is adequate. In this cross-sectional study, lumbar spine and femoral neck BMDs of 151 postmenopausal women aged 50 - 85 years were measured using dual-energy x-ray absorptiometry. Dietary intakes were assessed using a validated food frequency questionnaire. Renal net acid excretion (RNAE), an estimate of acid-base balance, was then calculated indirectly from the diet using the formulae of Remer (based on dietary intakes of protein, phosphorus, potassium, and magnesium; RNAERemer) and Frassetto (based on dietary intakes of protein and potassium; RNAEFrassetto), and was energy adjusted by the residual method. After adjusting for potential confounders, multivariable adjusted means of the lumbar spine BMD of women in the highest tertiles of RNAERemer and RNAEFrassetto were significantly lower than those in the lowest tertiles (for RNAERemer: mean difference -0.084 g/cm2; P=0.007 and for RNAEFrassetto: mean difference - 0.088 g/cm2; P=0.004). Similar results were observed in a subgroup analysis of subjects with dietary calcium intake of >800 mg/day. In conclusion, a higher RNAE (i. e. more dietary acidity), which is associated with greater intake of acid-generating foods and lower intake of alkali-generating foods, may be involved in deteriorating the bone health of postmenopausal Iranian women, even in the context of adequate dietary calcium intake.

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