T Remer1. 1. Research Institute of Child Nutrition--Forschungsinstitut für Kinderernährung--Department of Nutrition and Health, Dortmund, Germany. remer@fke-do.de
Abstract
BACKGROUND: Nutrition has long been known to strongly influence acid-base balance. Recently, we have shown that it is possible to appropriately estimate the renal net acid excretion (NAE) of healthy subjects from the composition of their diets. AIM OF THE STUDY: 1) To briefly present a physiologically based calculation model that allows a reasonable estimation of the analytically determined urinary NAE, 2) to summarize the underlying metabolic mechanisms and 3) to study the specific effect of protein on ammoniagenesis which may counteract, to a small degree, the primary acid load-increasing potential of protein. METHODS: The calculation model and the algorithm for predicting the dietary acid load are summarized, major metabolic (and intestinal) pathways of acid and base equivalents are explained, and urinary excretion rates of ammonium and NAE were specifically examined with special regard to the respective protein intake levels. For the latter examinations, data from diet experiments in adults and epidemiological data from children (protein intake; NAE, pH, and ammonium excretion in 24-h urine samples) were analyzed. RESULTS: The paper shows that the diet-induced generation of acidity and alkalinity is not only determined by the metabolism (oxidation) of sulfur-containing amino acids and organic acid anions of alkali salts, respectively. The intestine is also directly involved in the generation of food-derived acid or alkali loads which is due to the considerably different intestinal absorption rates of relevant food components, i. e., protein and minerals. Further analyses of the interrelation between diet and acid-base status revealed that increasing protein intake (despite its potential to increase NAE) also significantly improves the capacity for renal net acid excretion by stimulating urinary ammonium excretion. CONCLUSION: An adequate concept to estimate renal NAE and potential renal acid loads from dietary intakes must consider the specific bioavailability of the individual nutrients. Furthermore, an increased protein intake does not necessarily result in an accordingly increased use of endogenous acid excretion capacity for two reasons: 1) additional alkali loads in an appropriately composed diet can compensate for the protein-related raised acid production and 2) protein itself moderately improves the renal capacity to excrete net acid by increasing the endogenous supply of ammonia which is the major urinary hydrogen ion acceptor.
BACKGROUND: Nutrition has long been known to strongly influence acid-base balance. Recently, we have shown that it is possible to appropriately estimate the renal net acid excretion (NAE) of healthy subjects from the composition of their diets. AIM OF THE STUDY: 1) To briefly present a physiologically based calculation model that allows a reasonable estimation of the analytically determined urinary NAE, 2) to summarize the underlying metabolic mechanisms and 3) to study the specific effect of protein on ammoniagenesis which may counteract, to a small degree, the primary acid load-increasing potential of protein. METHODS: The calculation model and the algorithm for predicting the dietary acid load are summarized, major metabolic (and intestinal) pathways of acid and base equivalents are explained, and urinary excretion rates of ammonium and NAE were specifically examined with special regard to the respective protein intake levels. For the latter examinations, data from diet experiments in adults and epidemiological data from children (protein intake; NAE, pH, and ammonium excretion in 24-h urine samples) were analyzed. RESULTS: The paper shows that the diet-induced generation of acidity and alkalinity is not only determined by the metabolism (oxidation) of sulfur-containing amino acids and organic acid anions of alkali salts, respectively. The intestine is also directly involved in the generation of food-derived acid or alkali loads which is due to the considerably different intestinal absorption rates of relevant food components, i. e., protein and minerals. Further analyses of the interrelation between diet and acid-base status revealed that increasing protein intake (despite its potential to increase NAE) also significantly improves the capacity for renal net acid excretion by stimulating urinary ammonium excretion. CONCLUSION: An adequate concept to estimate renal NAE and potential renal acid loads from dietary intakes must consider the specific bioavailability of the individual nutrients. Furthermore, an increased protein intake does not necessarily result in an accordingly increased use of endogenous acid excretion capacity for two reasons: 1) additional alkali loads in an appropriately composed diet can compensate for the protein-related raised acid production and 2) protein itself moderately improves the renal capacity to excrete net acid by increasing the endogenous supply of ammonia which is the major urinary hydrogen ion acceptor.
Authors: I Alexandru Bobulescu; Naim M Maalouf; Giovanna Capolongo; Beverley Adams-Huet; Tara R Rosenthal; Orson W Moe; Khashayar Sakhaee Journal: Am J Physiol Renal Physiol Date: 2013-09-11
Authors: E-M Hietavala; J R Stout; J J Hulmi; H Suominen; H Pitkänen; R Puurtinen; H Selänne; H Kainulainen; A A Mero Journal: Eur J Clin Nutr Date: 2014-12-10 Impact factor: 4.016
Authors: Antti A Mero; Heikki Huovinen; Olle Matintupa; Juha J Hulmi; Risto Puurtinen; Hannele Hohtari; Tuomo Am Karila Journal: J Int Soc Sports Nutr Date: 2010-01-25 Impact factor: 5.150