High-Salt Diet Has a Certain Impact on Protein Digestion and Gut Microbiota: A Sequencing and Proteome Combined Study

Several studies have established a link between high-salt diet, inflammation, and hypertension. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut–kidney axis. We aimed to confirm the effects of high salt and calcitriol on the gut–kidney immune system and the composition of the intestinal flora. We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Calcitriol can reduce colon and kidney inflammation, and there are gene expression changes consistent with restored intestinal barrier function. The protective effect of calcitriol may be mediated indirectly by immunological properties. Additionally, the molecular pathways of the gut microbiota-mediated blood pressure regulation may be related to circadian rhythm signals, which needs to be further investigated. An innovative association analysis of the microbiota may be a key strategy to understanding the association between gene patterns and host.

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Su1901 High Salt Diet Increases Susceptibility to Experimental Colitis: A Putative Role of Gut Microbiota

Gastroenterology ◽

10.1016/s0016-5085(16)32000-5 ◽

2016 ◽

Vol 150 (4) ◽

pp. S583 ◽

Cited By ~ 2

Author(s):

Pedro M. Miranda ◽

Viktoria Serkis ◽

Giada de Palma ◽

Marc Pigrau ◽

Jun Lu ◽

...

Keyword(s):

Gut Microbiota ◽

Experimental Colitis ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Putative Role

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High-salt diet mediates interplay between NK cells and gut microbiota to induce potent tumor immunity

Science Advances ◽

10.1126/sciadv.abg5016 ◽

2021 ◽

Vol 7 (37) ◽

Author(s):

Zaigham Abbas Rizvi ◽

Rajdeep Dalal ◽

Srikanth Sadhu ◽

Yashwant Kumar ◽

Shakti Kumar ◽

...

Keyword(s):

Gut Microbiota ◽

Nk Cells ◽

Tumor Immunity ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Potent Tumor

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Berry-Enriched Diet in Salt-Sensitive Hypertensive Rats: Metabolic Fate of (Poly)Phenols and the Role of Gut Microbiota

Nutrients ◽

10.3390/nu11112634 ◽

2019 ◽

Vol 11 (11) ◽

pp. 2634 ◽

Cited By ~ 5

Author(s):

Gomes ◽

Oudot ◽

Macià ◽

Foito ◽

Carregosa ◽

...

Keyword(s):

Gut Microbiota ◽

High Salt ◽

In Vivo Model ◽

Microbiota Composition ◽

Metabolic Fate ◽

Hypertensive Rats ◽

High Salt Diet ◽

16S Rrna Analysis ◽

Salt Diet

Diets rich in (poly)phenols are associated with a reduced reduction in the incidence of cardiovascular disorders. While the absorption and metabolism of (poly)phenols has been described, it is not clear how their metabolic fate is affected under pathological conditions. This study evaluated the metabolic fate of berry (poly)phenols in an in vivo model of hypertension as well as the associated microbiota response. Dahl salt-sensitive rats were fed either a low-salt diet (0.26% NaCl) or a high-salt diet (8% NaCl), with or without a berry mixture (blueberries, blackberries, raspberries, Portuguese crowberry and strawberry tree fruit) for 9 weeks. The salt-enriched diet promoted an increase in the urinary excretion of berry (poly)phenol metabolites, while the abundance of these metabolites decreased in faeces, as revealed by UPLC–MS/MS. Moreover, salt and berries modulated gut microbiota composition as demonstrated by 16S rRNA analysis. Some changes in the microbiota composition were associated with the high-salt diet and revealed an expansion of the families Proteobacteria and Erysipelotrichaceae. However, this effect was mitigated by the dietary supplementation with berries. Alterations in the metabolic fate of (poly)phenols occur in parallel with the modulation of gut microbiota in hypertensive rats. Thus, beneficial effects of (poly)phenols could be related with these interlinked modifications, between metabolites and microbiota environments.

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Targeting the Gut Microbiota to Investigate the Mechanism of Lactulose in Negating the Effects of a High‐Salt Diet on Hypertension

Molecular Nutrition & Food Research ◽

10.1002/mnfr.201800941 ◽

2019 ◽

Vol 63 (11) ◽

pp. 1800941 ◽

Cited By ~ 11

Author(s):

Zheng Zhang ◽

Jiangtao Zhao ◽

Changyu Tian ◽

Xiao Chen ◽

Huan Li ◽

...

Keyword(s):

Gut Microbiota ◽

High Salt ◽

High Salt Diet ◽

Salt Diet

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Implantation and pregnancy outcome of rats fed with low and high salt diet

Endocrine Abstracts ◽

10.1530/endoabs.38.p361 ◽

2015 ◽

Author(s):

Iranloye Bolanle ◽

Oludare Gabriel

Keyword(s):

Pregnancy Outcome ◽

High Salt ◽

High Salt Diet ◽

Salt Diet

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463-P: Deterioration of Atherosclerosis via Dysbiosis in ApoE Null Mice Fed with High-Salt Diet

Diabetes ◽

10.2337/db20-463-p ◽

2020 ◽

Vol 69 (Supplement 1) ◽

pp. 463-P

Author(s):

TOMONORI KIMURA ◽

YOSHITAKA HASHIMOTO ◽

TAKAFUMI SENMARU ◽

EMI USHIGOME ◽

MASAHIDE HAMAGUCHI ◽

...

Keyword(s):

High Salt ◽

High Salt Diet ◽

Salt Diet

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Faculty Opinions recommendation of ET-1 increases reactive oxygen species following hypoxia and high-salt diet in the mouse glomerulus.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718876812.793503540 ◽

2015 ◽

Author(s):

Fredrik Palm

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

High Salt ◽

Oxygen Species ◽

High Salt Diet ◽

Salt Diet

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Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

International Journal of Molecular Sciences ◽

10.3390/ijms20143495 ◽

2019 ◽

Vol 20 (14) ◽

pp. 3495 ◽

Cited By ~ 1

Author(s):

Yanling Yan ◽

Jiayan Wang ◽

Muhammad A. Chaudhry ◽

Ying Nie ◽

Shuyan Sun ◽

...

Keyword(s):

Blood Pressure ◽

Renal Function ◽

Significant Rise ◽

Protein Carbonylation ◽

High Salt ◽

Kidney Cortex ◽

High Salt Diet ◽

Salt Diet ◽

Salt Sensitive Hypertension

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

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