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Sodium Intake and Related Diseases
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Sodium Intake and Related Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (20 December 2020) | Viewed by 48874

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editors

Prof. Dr. Pasquale Strazzullo

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Guest Editor
Department of Internal Medicine, University of Naples Federico II, Via S. Pansini 5, 80131, Naples, Italy
Interests: medicinal chemistry; hypertension; cardiovascular risk; cardiovascular diseases; nutrition; obesity.
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Antonello Santini

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Department of Pharmacy, University of Napoli Federico II, Via D. Montesano 49, 80131 Napoli, Italy
Interests: food chemistry; safety; food safety; food supplements and functional foods; nutraceuticals; sustainability; novel foods; nano-nutraceuticals; recovery from byproducts of the agri-food area; formulation and assessing of novel nutraceuticals; food contaminants; contaminants; risk assessment; mycotoxins and secondary metabolites; chemistry and food education
Special Issues, Collections and Topics in MDPI journals
Dr. Massimo Lucarini

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Guest Editor
CREA-Research Centre for Food and Nutrition, Via Ardeatina 546, 00178 Rome, Italy
Interests: natural compounds; nutraceuticals; natural products; food science and nutrition; food composition databases; bioaccesibility; dietary intake
Special Issues, Collections and Topics in MDPI journals
Dr. Alessandra Durazzo

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Guest Editor
CREA-Research Centre for Food and Nutrition, Via Ardeatina 546, 00178 Rome, Italy
Interests: bioactive compounds; natural products; nutraceuticals; antioxidants; dietary supplements; food quality; nutrition; food composition databases; bioavailability, metabolic pathway; nanoformulations
Special Issues, Collections and Topics in MDPI journals
Dr. Ginevra Lombardi-Boccia

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Consiglio per la ricerca in agricoltura e l’analisi dell’economia agraria – Centro di ricerca Alimenti e Nutrizione, Via Ardeatina 546, 00178 Rome, Italy
Interests: natural compounds; nutraceuticals; natural products; food science and nutrition; food composition databases; bioaccessibility; dietary intake; healthy diet
Special Issues, Collections and Topics in MDPI journals
Dr. Stefania Sette

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Guest Editor
CREA-Research Centre for Food and Nutrition, Via Ardeatina 546, 00178 Rome, Italy
Interests: data consumption; dietary intake; dietary survey; nutrition; foods; dietary supplements.

Special Issue Information

Dear Colleagues,

Moderation in the use of salt prevents the tendency of blood pressure to increase with age. In contrast, the abuse of salt frequently leads to increases in blood pressure and contributes to the development of hypertension, particularly in overweight or obese people, in diabetics, in the elderly and in genetically-predisposed subjects.

Given the well-known relationship between high blood pressure and the risk of cardiovascular disease, high salt consumption is also associated with an increased risk of fatal or otherwise debilitating cardiovascular events with a high impact on health expenditure.

The reduction of salt consumption leads to a decrease in blood pressure—more so in hypertensive, elderly and obese subjects—and consequently to a reduction in cardiovascular risk.

Significant associations have also been demonstrated between high salt consumption, the risk of gastric cancer (in particular in subjects with Helicobacter Pylori infection) and the risk of calcium nephrolithiasis (probably due to the increase in urinary calcium associated with high sodium intake).

The nutritional goal for the adult population has been set in not more than 2000 mg of sodium or 5 g of salt per day, in keeping with the WHO recommendation (2012) that applies to all adult individuals, including the elderly, in the absence of different medical/nutritional indications.

At least half of the amount of salt taken individually comes from processed foods and food purchased and/or consumed outside the home, which is why an effective reduction in salt consumption requires the active participation of the food industry and the constant attention of the consumer to the sodium content of the products purchased and consumed.

This Special Issue is focused on the role of sodium (salt) in the body's physiological processes. Generally, complex mechanisms regulate sodium concentrations in bodily fluids that involve the cardiovascular and endocrine systems, the central nervous system, and the autonomic nervous system. The mechanisms involved in the regulation of sodium homeostasis will be at the centre of this Special Issue. Some example topics are the mechanisms that influence the action of the sodium-potassium pump, the renal tubular reabsorption mechanisms regulated by hormones such as angiotensin II and norepinephrine and those of elimination, regulated by dopamine and cyclic AMP. The mechanisms involved at the molecular level of the relationship between sodium intake–blood pressure–cardiovascular disease, and stomach cancer, will be one of the focuses of the Special Issue.

The main topics include, but are not limited to:

  • Levels of intake and main sources of sodium from the diet: effect on the health status and description of the biochemical processes involved;
  • Salt and related risks. Studies in the management and treatment of sodium intake-related diseases;
  • Epidemiological studies of the relationship between salt intake and related diseases: focus on the mechanism of action;
  • Delineation of mechanism of actions: in vitro and in vivo studies.
  • Salt and sapidity: mechanisms of taste perception.

Dr. Alessandra Durazzo
Dr. Massimo Lucarini
Prof. Dr. Antonello Santini
Prof. Pasquale Strazzullo
Dr. Ginevra Lombardi-Boccia
Dr. Stefania Sette
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • sodium
  • salt
  • food sources
  • intake levels
  • in vitro and in vivo studies
  • mechanisms of action
  • epidemiological studies
  • salt replaces
  • technological solutions
  • community strategies

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Published Papers (6 papers)

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Editorial

Jump to: Research, Review

3 pages, 168 KiB  
Editorial
Sodium Intake and Related Diseases
by Massimo Lucarini, Alessandra Durazzo, Stefania Sette, Ginevra Lombardi-Boccia, Antonello Santini and Pasquale Strazzullo
Int. J. Mol. Sci. 2021, 22(14), 7608; https://doi.org/10.3390/ijms22147608 - 16 Jul 2021
Cited by 6 | Viewed by 2249
Abstract
Moderation in the use of salt (sodium chloride) in food and food preparations prevents the tendency of blood pressure to increase with age, and this is documented by many studies in current literature [...] Full article
(This article belongs to the Special Issue Sodium Intake and Related Diseases)

Research

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16 pages, 3622 KiB  
Article
MST3 Involvement in Na+ and K+ Homeostasis with Increasing Dietary Potassium Intake
by Chee-Hong Chan, Sheng-Nan Wu, Bo-Ying Bao, Houng-Wei Li and Te-Ling Lu
Int. J. Mol. Sci. 2021, 22(3), 999; https://doi.org/10.3390/ijms22030999 - 20 Jan 2021
Cited by 5 | Viewed by 2315
Abstract
K+ loading inhibits NKCC2 (Na-K-Cl cotransporter) and NCC (Na-Cl cotransporter) in the early distal tubules, resulting in Na+ delivery to the late distal convoluted tubules (DCTs). In the DCTs, Na+ entry through ENaC (epithelial Na channel) drives K+ secretion [...] Read more.
K+ loading inhibits NKCC2 (Na-K-Cl cotransporter) and NCC (Na-Cl cotransporter) in the early distal tubules, resulting in Na+ delivery to the late distal convoluted tubules (DCTs). In the DCTs, Na+ entry through ENaC (epithelial Na channel) drives K+ secretion through ROMK (renal outer medullary potassium channel). WNK4 (with-no-lysine 4) regulates the NCC/NKCC2 through SAPK (Ste20-related proline-alanine-rich kinase)/OSR1 (oxidative stress responsive). K+ loading increases intracellular Cl−, which binds to the WNK4, thereby inhibiting autophosphorylation and downstream signals. Acute K+ loading-deactivated NCC was not observed in Cl−-insensitive WNK4 mice, indicating that WNK4 was involved in K+ loading-inhibited NCC activity. However, chronic K+ loading deactivated NCC in Cl−-insensitive WNK4 mice, indicating that other mechanisms may be involved. We previously reported that mammalian Ste20-like protein kinase 3 (MST3/STK24) was expressed mainly in the medullary TAL (thick ascending tubule) and at lower levels in the DCTs. MST3−/− mice exhibited higher ENaC activity, causing hypernatremia and hypertension. To investigate MST3 function in maintaining Na+/K+ homeostasis in kidneys, mice were fed diets containing various concentrations of Na+ and K+. The 2% KCl diets induced less MST3 expression in MST3−/− mice than that in wild-type (WT) mice. The MST3−/− mice had higher WNK4, NKCC2-S130 phosphorylation, and ENaC expression, resulting in lower urinary Na+ and K+ excretion than those of WT mice. Lower urinary Na+ excretion was associated with elevated plasma [Na+] and hypertension. These results suggest that MST3 maintains Na+/K+ homeostasis in response to K+ loading by regulation of WNK4 expression and NKCC2 and ENaC activity. Full article
(This article belongs to the Special Issue Sodium Intake and Related Diseases)
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14 pages, 2227 KiB  
Article
PGI2 Analog Attenuates Salt-Induced Renal Injury through the Inhibition of Inflammation and Rac1-MR Activation
by Daigoro Hirohama, Wakako Kawarazaki, Mitsuhiro Nishimoto, Nobuhiro Ayuzawa, Takeshi Marumo, Shigeru Shibata and Toshiro Fujita
Int. J. Mol. Sci. 2020, 21(12), 4433; https://doi.org/10.3390/ijms21124433 - 22 Jun 2020
Cited by 9 | Viewed by 3112
Abstract
Renal inflammation is known to be involved in salt-induced renal damage, leading to end-stage renal disease. This study aims to evaluate the role of inflammation in anti-inflammatory and renoprotective effects of beraprost sodium (BPS), a prostaglandin I2 (PGI2) analog, in [...] Read more.
Renal inflammation is known to be involved in salt-induced renal damage, leading to end-stage renal disease. This study aims to evaluate the role of inflammation in anti-inflammatory and renoprotective effects of beraprost sodium (BPS), a prostaglandin I2 (PGI2) analog, in Dahl salt-sensitive (DS) rats. Five-week-old male DS rats were fed a normal-salt diet (0.5% NaCl), a high-salt diet (8% NaCl), or a high-salt diet plus BPS treatment for 3 weeks. BPS treatment could inhibit marked proteinuria and renal injury in salt-loaded DS rats with elevated blood pressure, accompanied by renal inflammation suppression. Notably, high salt increased renal expression of active Rac1, followed by increased Sgk1 expressions, a downstream molecule of mineralocorticoid receptor (MR) signal, indicating salt-induced activation of Rac1-MR pathway. However, BPS administration inhibited salt-induced Rac1-MR activation as well as renal inflammation and damage, suggesting that Rac1-MR pathway is involved in anti-inflammatory and renoprotective effects of PGI2. Based upon Rac1 activated by inflammation, moreover, BPS inhibited salt-induced activation of Rac1-MR pathway by renal inflammation suppression, resulting in the attenuation of renal damage in salt-loaded DS rats. Thus, BPS is efficacious for the treatment of salt-induced renal injury. Full article
(This article belongs to the Special Issue Sodium Intake and Related Diseases)
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21 pages, 2661 KiB  
Article
Na+-Coupled Nutrient Cotransport Induced Luminal Negative Potential and Claudin-15 Play an Important Role in Paracellular Na+ Recycling in Mouse Small Intestine
by Michiko Nakayama, Noriko Ishizuka, Wendy Hempstock, Akira Ikari and Hisayoshi Hayashi
Int. J. Mol. Sci. 2020, 21(2), 376; https://doi.org/10.3390/ijms21020376 - 7 Jan 2020
Cited by 8 | Viewed by 4877
Abstract
Many nutrients are absorbed via Na+ cotransport systems, and therefore it is predicted that nutrient absorption mechanisms require a large amount of luminal Na+. It is thought that Na+ diffuses back into the lumen via paracellular pathways to support [...] Read more.
Many nutrients are absorbed via Na+ cotransport systems, and therefore it is predicted that nutrient absorption mechanisms require a large amount of luminal Na+. It is thought that Na+ diffuses back into the lumen via paracellular pathways to support Na+ cotransport absorption. However, direct experimental evidence in support of this mechanism has not been shown. To elucidate this, we took advantage of claudin-15 deficient (cldn15−/−) mice, which have been shown to have decreased paracellular Na+ permeability. We measured glucose-induced currents (ΔIsc) under open- and short-circuit conditions and simultaneously measured changes in unidirectional 22Na+ fluxes (ΔJNa) in Ussing chambers. Under short-circuit conditions, application of glucose resulted in an increase in ΔIsc and unidirectional mucosal to serosal 22Na+ (∆JNaMS) flux in both wild-type and cldn15−/− mice. However, under open-circuit conditions, ΔIsc was observed but ∆JNaMS was strongly inhibited in wild-type but not in cldn15−/− mice. In addition, in the duodenum of mice treated with cholera toxin, paracellular Na+ conductance was decreased and glucose-induced ∆JNaMS increment was observed under open-circuit conditions. We concluded that the Na+ which is absorbed by Na+-dependent glucose cotransport is recycled back into the lumen via paracellular Na+ conductance through claudin-15, which is driven by Na+ cotransport induced luminal negativity. Full article
(This article belongs to the Special Issue Sodium Intake and Related Diseases)
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Review

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12 pages, 587 KiB  
Review
Sodium Intake and Heart Failure
by Yash Patel and Jacob Joseph
Int. J. Mol. Sci. 2020, 21(24), 9474; https://doi.org/10.3390/ijms21249474 - 13 Dec 2020
Cited by 74 | Viewed by 18298
Abstract
Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy [...] Read more.
Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure. Full article
(This article belongs to the Special Issue Sodium Intake and Related Diseases)
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13 pages, 484 KiB  
Review
Sodium Intake and Chronic Kidney Disease
by Silvio Borrelli, Michele Provenzano, Ida Gagliardi, Ashour Michael, Maria Elena Liberti, Luca De Nicola, Giuseppe Conte, Carlo Garofalo and Michele Andreucci
Int. J. Mol. Sci. 2020, 21(13), 4744; https://doi.org/10.3390/ijms21134744 - 3 Jul 2020
Cited by 82 | Viewed by 16322
Abstract
In Chronic Kidney Disease (CKD) patients, elevated blood pressure (BP) is a frequent finding and is traditionally considered a direct consequence of their sodium sensitivity. Indeed, sodium and fluid retention, causing hypervolemia, leads to the development of hypertension in CKD. On the other [...] Read more.
In Chronic Kidney Disease (CKD) patients, elevated blood pressure (BP) is a frequent finding and is traditionally considered a direct consequence of their sodium sensitivity. Indeed, sodium and fluid retention, causing hypervolemia, leads to the development of hypertension in CKD. On the other hand, in non-dialysis CKD patients, salt restriction reduces BP levels and enhances anti-proteinuric effect of renin–angiotensin–aldosterone system inhibitors in non-dialysis CKD patients. However, studies on the long-term effect of low salt diet (LSD) on cardio-renal prognosis showed controversial findings. The negative results might be the consequence of measurement bias (spot urine and/or single measurement), reverse epidemiology, as well as poor adherence to diet. In end-stage kidney disease (ESKD), dialysis remains the only effective means to remove dietary sodium intake. The mismatch between intake and removal of sodium leads to fluid overload, hypertension and left ventricular hypertrophy, therefore worsening the prognosis of ESKD patients. This imposes the implementation of a LSD in these patients, irrespective of the lack of trials proving the efficacy of this measure in these patients. LSD is, therefore, a rational and basic tool to correct fluid overload and hypertension in all CKD stages. The implementation of LSD should be personalized, similarly to diuretic treatment, keeping into account the volume status and true burden of hypertension evaluated by ambulatory BP monitoring. Full article
(This article belongs to the Special Issue Sodium Intake and Related Diseases)
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