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Influence of Nutrients on Acid-Base Balance

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (1 October 2020) | Viewed by 12321

Special Issue Editor


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Guest Editor
Department of Clinical Medicine and Surgery, ESH Excellence Center of Hypertension, and Internal Medicine and Clinical Nutrition Unit, Federico II University Hospital of Naples, Via S. Pansini 5, 80131 Naples, Italy
Interests: trace elements; vitamins; nutrition; artificial nutrition; malnutrition; parenteral nutrition; enteral nutrition; cardiovascular diseases; obesity; amino acids; bone health; skeletal muscle mass; hypertension; physicochemical stability of all-in-one parenteral nutrition mixtures; membrane ion transport systems; genetic aspects of atherosclerosis, hypertension, and obesity

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide the most updated clinical evidence concerning the relationship between food carrying acid-forming nutrients and chronic and metabolic disorders, and also related mechanisms in their progression. Nutrients are known to influence the body's acid–base balance, providing precursors of non-volatile acids and bases. Diets high in acid-forming nutrients induce a chronic low-grade metabolic acidosis status jointly with the progress of metabolic alterations such as insulin resistance, diabetes, metabolic bone disease, chronic kidney disease, age-related muscle loss, hypertension, and other chronic diseases. Beyond the general population, this Special Issue is also of interest to long-term artificial nutrition patients. Metabolic acidosis and metabolic bone disease are frequent complications in patients receiving total parenteral or enteral nutrition due to the excessive exogenous administration and/or endogenous production of non-volatile acids.

Submissions of experimental papers, up-to-date reviews (systematic reviews and meta-analyses), and commentaries addressing a broad range of issues related to this topic are welcome.

I look forward to your stimulant submissions.

Dr. Roberto Iacone
Guest Editor

Manuscript Submission Information

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Keywords

  • Acid–base balance
  • Potential renal acid load
  • Net acid excretion
  • Metabolic acidosis
  • Chronic low-grade metabolic acidosis
  • Acid alkaline diet
  • Acid-forming nutrients
  • Base-forming nutrients
  • Fruits and vegetables
  • Metabolic bone disease
  • Osteoporosis
  • Cardiovascular disease
  • Hypertension
  • Chronic kidney disease
  • Insulin resistance
  • Diabetes
  • Muscle mass loss
  • Artificial nutrition
  • Parenteral nutrition
  • Enteral nutrition

Published Papers (3 papers)

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Research

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24 pages, 37855 KiB  
Article
Citrate Supplementation Restores the Impaired Mineralisation Resulting from the Acidic Microenvironment: An In Vitro Study
by Francesca Perut, Gabriela Graziani, Marta Columbaro, Renata Caudarella, Nicola Baldini and Donatella Granchi
Nutrients 2020, 12(12), 3779; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12123779 - 09 Dec 2020
Cited by 2 | Viewed by 2265
Abstract
Chronic metabolic acidosis leads to bone-remodelling disorders based on excessive mineral matrix resorption and inhibition of bone formation, but also affects the homeostasis of citrate, which is an essential player in maintaining the acid–base balance and in driving the mineralisation process. This study [...] Read more.
Chronic metabolic acidosis leads to bone-remodelling disorders based on excessive mineral matrix resorption and inhibition of bone formation, but also affects the homeostasis of citrate, which is an essential player in maintaining the acid–base balance and in driving the mineralisation process. This study aimed to investigate the impact of acidosis on the osteogenic properties of bone-forming cells and the effects of citrate supplementation in restoring the osteogenic features impaired by the acidic milieu. For this purpose, human mesenchymal stromal cells were cultured in an osteogenic medium and the extracellular matrix mineralisation was analysed at the micro- and nano-level, both in neutral and acidic conditions and after treatment with calcium citrate and potassium citrate. The acidic milieu significantly decreased the citrate release and hindered the organisation of the extracellular matrix, but the citrate supplementation increased collagen production and, particularly calcium citrate, promoted the mineralisation process. Moreover, the positive effect of citrate supplementation was observed also in the physiological microenvironment. This in vitro study proves that the mineral matrix organisation is influenced by citrate availability in the microenvironment surrounding bone-forming cells, thus providing a biological basis for using citrate-based supplements in the management of bone-remodelling disorders related to chronic low-grade acidosis. Full article
(This article belongs to the Special Issue Influence of Nutrients on Acid-Base Balance)
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18 pages, 2414 KiB  
Article
Effects of an Alkalizing or Acidizing Diet on High-Intensity Exercise Performance under Normoxic and Hypoxic Conditions in Physically Active Adults: A Randomized, Crossover Trial
by Mirjam Limmer, Juliane Sonntag, Markus de Marées and Petra Platen
Nutrients 2020, 12(3), 688; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12030688 - 04 Mar 2020
Cited by 5 | Viewed by 4711
Abstract
Pre-alkalization caused by dietary supplements such as sodium bicarbonate improves anaerobic exercise performance. However, the influence of a base-forming nutrition on anaerobic performance in hypoxia remains unknown. Herein, we investigated the effects of an alkalizing or acidizing diet on high-intensity performance and associated [...] Read more.
Pre-alkalization caused by dietary supplements such as sodium bicarbonate improves anaerobic exercise performance. However, the influence of a base-forming nutrition on anaerobic performance in hypoxia remains unknown. Herein, we investigated the effects of an alkalizing or acidizing diet on high-intensity performance and associated metabolic parameters in normoxia and hypoxia. In a randomized crossover design, 15 participants (24.5 ± 3.9 years old) performed two trials following four days of either an alkalizing (BASE) or an acidizing (ACID) diet in normoxia. Subsequently, participants performed two trials (BASE; ACID) after 12 h of normobaric hypoxic exposure. Anaerobic exercise performance was assessed using the portable tethered sprint running (PTSR) test. PTSR assessed overall peak force, mean force, and fatigue index. Blood lactate levels, blood gas parameters, heart rate, and rate of perceived exertion were assessed post-PTSR. Urinary pH was analyzed daily. There were no differences between BASE and ACID conditions for any of the PTSR-related parameters. However, urinary pH, blood pH, blood bicarbonate concentration, and base excess were significantly higher in BASE compared with ACID (p < 0.001). These findings show a diet-induced increase in blood buffer capacity, represented by blood bicarbonate concentration and base excess. However, diet-induced metabolic changes did not improve PTSR-related anaerobic performance. Full article
(This article belongs to the Special Issue Influence of Nutrients on Acid-Base Balance)
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Review

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10 pages, 777 KiB  
Review
Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review
by Giulia C. Signorelli, Mario G. Bianchetti, Luca M. M. Jermini, Carlo Agostoni, Gregorio P. Milani, Giacomo D. Simonetti and Sebastiano A. G. Lava
Nutrients 2020, 12(11), 3436; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12113436 - 09 Nov 2020
Cited by 6 | Viewed by 4699
Abstract
Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and [...] Read more.
Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and acid–base abnormality. In patients with excessive loss of salt in the sweat or poor salt intake, the maintenance of metabolic alkalosis is crucially modulated by the chloride–bicarbonate exchanger pendrin located on the renal tubular membrane of type B intercalated cells. In the late 1970s, recommendations were made to decrease the salt content of foods as part of an effort to minimize the tendency towards systemic hypertension. Hence, the baby food industry decided to remove added salt from formula milk. Some weeks later, approximately 200 infants (fed exclusively with formula milks with a chloride content of only 2–4 mmol/L), were admitted with failure to thrive, constipation, food refusal, muscular weakness, and delayed psychomotor development. The laboratory work-up disclosed metabolic alkalosis, hypokalemia, hypochloremia, and a reduced urinary chloride excretion. In all cases, both the clinical and the laboratory features remitted in ≤7 days when the infants were fed on formula milk with a normal chloride content. Since 1982, 13 further publications reported additional cases of dietary chloride depletion. It is therefore concluded that the dietary intake of chloride, which was previously considered a “mendicant” ion, plays a crucial role in acid–base and salt balance. Full article
(This article belongs to the Special Issue Influence of Nutrients on Acid-Base Balance)
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