Beetroot and Sodium Nitrate Ameliorate Cardiometabolic Changes in Diet‐Induced Obese Hypertensive Rats

Bhaswant, Maharshi; Brown, Lindsay; McAinch, Andrew J.; Mathai, Michael L.

doi:10.1002/mnfr.201700478

Cited by 26 publications

(16 citation statements)

References 63 publications

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“…50 As nitrate can be metabolized to nitrite and also exert antioxidant effects, it is possible that it causes similar effects as compared to those associated with nitrite therapy in order to reduce MMP-2 activity in hypertension. In fact, it has already been demonstrated that nitrate can revert the increase in MMP-2 expression caused by a high-fat diet, 59 although the mechanism explaining nitrite-induced MMP inhibition is not entirely known. Under inflammatory conditions, MMP-9 expression and activity are down-regulated by S-nitrosothiols in bronchial epithelial cells.…”

Section: Nitrate and Nitrite Reduce Cardiovascular Remodelling In Hmentioning

confidence: 99%

Nitrate and nitrite‐based therapy to attenuate cardiovascular remodelling in arterial hypertension

Guimaraes

Batista

Tanus‐Santos

2020

Basic Clin Pharma Tox

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Elevated blood pressure is a leading global contributor to death and disability worldwide, and in 2010, about 1.4 billion people were hypertensive. 1 Hypertension involves a complex interplay of environmental and pathophysiological factors that affect multiple systems and is the most common risk factor that predisposes to cardiovascular diseases. 2 Through its effects on target organs, hypertension has been associated with a variety of cardiovascular comorbidities such as coronary artery disease, stroke, chronic kidney disease, metabolic syndrome and dyslipidaemia. 3 Maintenance of normal blood pressure is dependent on the balance between the cardiac output and vascular resistance.

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Section: Nitrate and Nitrite Reduce Cardiovascular Remodelling In Hmentioning

confidence: 99%

Nitrate and nitrite‐based therapy to attenuate cardiovascular remodelling in arterial hypertension

Guimaraes

Batista

Tanus‐Santos

2020

Basic Clin Pharma Tox

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“…Notably, NO donors facilitate glucose transport in skeletal muscles via the stimulation of glucose transporter type 4 abundance: an important regulatory step for glucose uptake in skeletal muscle, heart, and adipose tissue (17–19). Long-term nitrate deficiency is associated with glucose intolerance, hyperglycemia, and an increased risk of atherosclerosis in mice (20), while the supplementation of nitrate-deficient diets with nitrate improves glucose tolerance, insulin resistance, and dyslipidemia in rodent models of hyperglycemia and diet-induced obesity (21, 22). These findings are consistent with the concept that dietary nitrate may be an essential nutrient (20, 23, 24).…”

Section: Introductionmentioning

confidence: 99%

Treatment with Nitrate, but Not Nitrite, Lowers the Oxygen Cost of Exercise and Decreases Glycolytic Intermediates While Increasing Fatty Acid Metabolites in Exercised Zebrafish

Axton

Beaver

Mary

et al. 2019

The Journal of Nutrition

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Background Dietary nitrate improves exercise performance by reducing the oxygen cost of exercise, although the mechanisms responsible are not fully understood. Objectives We tested the hypothesis that nitrate and nitrite treatment would lower the oxygen cost of exercise by improving mitochondrial function and stimulating changes in the availability of metabolic fuels for energy production. Methods We treated 9-mo-old zebrafish with nitrate (sodium nitrate, 606.9 mg/L), nitrite (sodium nitrite, 19.5 mg/L), or control (no treatment) water for 21 d. We measured oxygen consumption during a 2-h, strenuous exercise test; assessed the respiration of skeletal muscle mitochondria; and performed untargeted metabolomics on treated fish, with and without exercise. Results Nitrate and nitrite treatment increased blood nitrate and nitrite levels. Nitrate treatment significantly lowered the oxygen cost of exercise, as compared with pretreatment values. In contrast, nitrite treatment significantly increased oxygen consumption with exercise. Nitrate and nitrite treatments did not change mitochondrial function measured ex vivo, but significantly increased the abundances of ATP, ADP, lactate, glycolytic intermediates (e.g., fructose 1,6-bisphosphate), tricarboxylic acid (TCA) cycle intermediates (e.g., succinate), and ketone bodies (e.g., β-hydroxybutyrate) by 1.8- to 3.8-fold, relative to controls. Exercise significantly depleted glycolytic and TCA intermediates in nitrate- and nitrite-treated fish, as compared with their rested counterparts, while exercise did not change, or increased, these metabolites in control fish. There was a significant net depletion of fatty acids, acyl carnitines, and ketone bodies in exercised, nitrite-treated fish (2- to 4-fold), while exercise increased net fatty acids and acyl carnitines in nitrate-treated fish (1.5- to 12-fold), relative to their treated and rested counterparts. Conclusions Nitrate and nitrite treatment increased the availability of metabolic fuels (ATP, glycolytic and TCA intermediates, lactate, and ketone bodies) in rested zebrafish. Nitrate treatment may improve exercise performance, in part, by stimulating the preferential use of fuels that require less oxygen for energy production.

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“…nitric oxide synthase (NOS)-independent mechanism, to increase NO production 7,8 . Importantly, this strategy has been shown to have therapeutic cardioprotective effects in other pre-clinical models of cardiomyopathy [9][10][11][12][13][14] . Pertinent to DOX-induced cardiomyopathy, two foundational studies have been conducted exploring the cardioprotective potential of SN co-supplementation.…”

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confidence: 99%

Sodium nitrate co-supplementation does not exacerbate low dose metronomic doxorubicin-induced cachexia in healthy mice

Campelj

Debruin

Timpani

et al. 2020

Sci Rep

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The purpose of this study was to determine whether (1) sodium nitrate (SN) treatment progressed or alleviated doxorubicin (DOX)-induced cachexia and muscle wasting; and (2) if a more-clinically relevant low-dose metronomic (LDM) DOX treatment regimen compared to the high dosage bolus commonly used in animal research, was sufficient to induce cachexia in mice. Six-week old male Balb/C mice (n = 16) were treated with three intraperitoneal injections of either vehicle (0.9% NaCl; VEH) or DOX (4 mg/kg) over one week. To test the hypothesis that sodium nitrate treatment could protect against DOX-induced symptomology, a group of mice (n = 8) were treated with 1 mM NaNO3 in drinking water during DOX (4 mg/kg) treatment (DOX + SN). Body composition indices were assessed using echoMRI scanning, whilst physical and metabolic activity were assessed via indirect calorimetry, before and after the treatment regimen. Skeletal and cardiac muscles were excised to investigate histological and molecular parameters. LDM DOX treatment induced cachexia with significant impacts on both body and lean mass, and fatigue/malaise (i.e. it reduced voluntary wheel running and energy expenditure) that was associated with oxidative/nitrostative stress sufficient to induce the molecular cytotoxic stress regulator, nuclear factor erythroid-2-related factor 2 (NRF-2). SN co-treatment afforded no therapeutic potential, nor did it promote the wasting of lean tissue. Our data re-affirm a cardioprotective effect for SN against DOX-induced collagen deposition. In our mouse model, SN protected against LDM DOX-induced cardiac fibrosis but had no effect on cachexia at the conclusion of the regimen.

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Beetroot and Sodium Nitrate Ameliorate Cardiometabolic Changes in Diet‐Induced Obese Hypertensive Rats

Abstract: The similar functional and molecular responses to beetroot and sodium nitrate indicate that the nitrate content of beetroot reduced inflammation and improved cardiovascular, liver, and metabolic function in rats with metabolic syndrome, rather than betanin.

Cited by 26 publications

References 63 publications

Nitrate and nitrite‐based therapy to attenuate cardiovascular remodelling in arterial hypertension

Nitrate and nitrite‐based therapy to attenuate cardiovascular remodelling in arterial hypertension

Treatment with Nitrate, but Not Nitrite, Lowers the Oxygen Cost of Exercise and Decreases Glycolytic Intermediates While Increasing Fatty Acid Metabolites in Exercised Zebrafish

Sodium nitrate co-supplementation does not exacerbate low dose metronomic doxorubicin-induced cachexia in healthy mice

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