scholarly journals Restructuring the Gut Microbiota by Intermittent Fasting Lowers Blood Pressure

2021 ◽  
Author(s):  
Huanan Shi ◽  
Bojun Zhang ◽  
Taylor Abo-Hamzy ◽  
James W Nelson ◽  
Chandra Shekar R Ambati ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gut Microbiota ◽  
Intermittent Fasting ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects ◽  
Gut Dysbiosis ◽  
Hypertension Prevention ◽  
Plasma Metabolome ◽  
Genome Shotgun Sequence ◽  
G Protein Coupled

Raionale: : In recent years, it has been demonstrated that a pathological change in the gut microbiota, termed gut dysbiosis, can be an underlying factor for the development of hypertension. Prevention of this dysbiosis can attenuate or abolish hypertension. Translational mechanisms to prevent gut dysbiosis as well as understanding of the mechanisms linking gut dysbiosis to hypertension are lacking. Objective: We first examined the efficacy of intermittent fasting (IF) in altering the gut microbiota and lowering blood pressure (BP). Next, we utilized a multi-omics approach to examine microbial influenced metabolites that may serve as the link between the gut microbiota and host BP regulation. Methods and Results: We demonstrate that IF significantly altered the makeup of the gut microbiota, cecal and plasma metabolome, and prevented the development of hypertension in the spontaneously hypertensive stroke-prone rat (SHRSP). The beneficial effects of IF were shown to be due to alterations of the gut microbiota through germ-free (GF) transplantation studies. GF rats receiving microbiota from IF SHRSP had significantly lower BP as compared to GF rats receiving microbiota from ad libitum fed SHRSPs. Through whole genome shotgun sequence analysis of the microbiota and untargeted metabolomics of cecal content and plasma we identified bile acid (BA) metabolism as a potential mediator in BP regulation. Finally, we show supplementation with cholic acid, or activation of the G protein-coupled BA receptor (TGR5), significantly reduced BP of the SHRSP. Conclusions: These studies demonstrate the BP lowering effects of IF involves manipulation of the gut microbiota and metabolome, and implicates disrupted BA signaling as novel mechanisms by which gut dysbiosis contributes to hypertension.

scholarly journals Alterations in the gut microbiota can elicit hypertension in rats

2017 ◽  
Vol 49 (2) ◽  
pp. 96-104 ◽  
Author(s):  
Sareema Adnan ◽  
James W. Nelson ◽  
Nadim J. Ajami ◽  
Venugopal R. Venna ◽  
Joseph F. Petrosino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gut Microbiota ◽  
Systolic Blood Pressure ◽  
Ribosomal Rna ◽  
Shr Rats ◽  
Spontaneously Hypertensive ◽  
Gut Dysbiosis ◽  
16S Ribosomal Rna Gene ◽  
Previously Treated ◽  
Normotensive Strain

Gut dysbiosis has been linked to cardiovascular diseases including hypertension. We tested the hypothesis that hypertension could be induced in a normotensive strain of rats or attenuated in a hypertensive strain of rats by exchanging the gut microbiota between the two strains. Cecal contents from spontaneously hypertensive stroke prone rats (SHRSP) were pooled. Similarly, cecal contents from normotensive WKY rats were pooled. Four-week-old recipient WKY and SHR rats, previously treated with antibiotics to reduce the native microbiota, were gavaged with WKY or SHRSP microbiota, resulting in four groups; WKY with WKY microbiota (WKY g-WKY), WKY with SHRSP microbiota (WKY g-SHRSP), SHR with SHRSP microbiota (SHR g-SHRSP), and SHR with WKY microbiota (SHR g-WKY). Systolic blood pressure (SBP) was measured weekly using tail-cuff plethysmography. At 11.5 wk of age systolic blood pressure increased 26 mmHg in WKY g-SHRSP compared with that in WKY g-WKY (182 ± 8 vs. 156 ± 8 mmHg, P = 0.02). Although the SBP in SHR g-WKY tended to decrease compared with SHR g-SHRSP, the differences were not statistically significant. Fecal pellets were collected at 11.5 wk of age for identification of the microbiota by sequencing the 16S ribosomal RNA gene. We observed a significant increase in the Firmicutes:Bacteroidetes ratio in the hypertensive WKY g-SHRSP, as compared with the normotensive WKY g-WKY ( P = 0.042). Relative abundance of multiple taxa correlated with SBP. We conclude that gut dysbiosis can directly affect SBP. Manipulation of the gut microbiota may represent an innovative treatment for hypertension.

Abstract P241: Intermittent Fasting Lowers Blood Pressure In A Rat Model Of Hypertension By Modulating The Gut Microbiota

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Huanan Shi ◽  
Taylor Abo-Hamzy ◽  
Robert M Bryan ◽  
David J Durgan
Keyword(s):  
Blood Pressure ◽  
Gut Microbiota ◽  
Intermittent Fasting ◽  
Microbial Metabolites ◽  
Targeted Metabolomics ◽  
Oral Gavage ◽  
Spontaneously Hypertensive ◽  
Germ Free ◽  
Wistar Kyoto ◽  
Principle Coordinate Analysis

Studies have demonstrated that disruption of the gut microbiota, termed gut dysbiosis, plays a causal role in the development of hypertension (HT) in animal models and patients. Recent studies revealed that intermittent fasting alters the gut microbiota and the production of microbial metabolites. Thus, we hypothesized that every-other-day-fasting (EODF) would prevent elevations of blood pressure (BP) in spontaneously hypertensive stroke prone rat (SHRSP) by maintaining a healthy gut microbiota. Five-week old SHRSP rats and normotensive Wistar Kyoto (WKY) rats were randomized to be fed ad lib or on EODF for 10 weeks. BP was measured weekly, and cecal content and plasma were collected at the end of the study. To examine the roles of gut microbiota and microbial metabolites in hypertension, we performed whole-genome shotgun sequencing on cecal samples and non-targeted metabolomics on cecal contents and plasma. To examine the direct effects of the EODF altered microbiota on BP regulation and eliminate the confounding variable of fasting, pooled cecal contents of SHRSP and WKY animals fed ad lib or EODF were given to germ free (GF) rats by oral gavage. We found that ten-weeks EODF was able to prevent elevations of systolic BP (SBP) in SHRSP compared to ad lib fed SHRSP (~220 vs. ~170mmHg; n=6-8, p<0.05), and that germ free rats transplanted with SHRSP ad lib microbiota had a significantly higher SBP as compared to those transplanted with SHRSP EODF microbiota (~152 vs. ~140 mmHg; n=6-7, p<0.01), indicating that microbiota and their metabolites are accountable for the effects of EODF. Principle coordinate analysis showed that EODF significantly altered the overall composition of both WKY and SHRSP microbiota (WKY p<0.01, SHRSP p<0.009). Multi-omics analysis indicates distinct microbiome and metabolome in SHRSP compared to WKY, and significant alterations to each induced by EODF. These findings suggest that EODF is able to prevent hypertension in SHRSP, and this involves altering the gut microbiota and metabolome.

Probiotic yogurt blunts the increase of blood pressure in spontaneously hypertensive rats via remodeling gut microbiota

2021 ◽  
Author(s):  
lishun wang ◽  
chaoyue kong ◽  
zhanming li ◽  
yuqin mao ◽  
bing han ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gut Microbiota ◽  
Dietary Intake ◽  
Lower Incidence ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects ◽  
Probiotic Yogurt

Dietary intake of probiotic yogurt, which has beneficial effects on intestinal microecology, is associated with a lower incidence of hypertension. Recent studies have shown that the gut microbiota plays a...

scholarly journals Dehulled Adlay Consumption Modulates Blood Pressure in Spontaneously Hypertensive Rats and Overweight and Obese Young Adults

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2305
Author(s):  
Wan-Ju Yeh ◽  
Jung Ko ◽  
Wei-Yi Cheng ◽  
Hsin-Yi Yang
Keyword(s):  
Blood Pressure ◽  
Daily Intake ◽  
Experimental Period ◽  
Overweight And Obesity ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects ◽  
Underlying Mechanisms ◽  
Grain Foods

High blood pressure is a crucial risk factor for many cardiovascular diseases, and a diet rich in whole-grain foods may modulate blood pressure. This study investigated the effects of dehulled adlay consumption on blood pressure in vivo. We initially fed spontaneous hypertensive rats diets without (SHR group) or with 12 or 24% dehulled adlay (SHR + LA and SHR + HA groups), and discovered that it could limit blood pressure increases over a 12-week experimental period. Although we found no significant changes in plasma, heart, and kidney angiotensin-converting enzyme activities, both adlay-consuming groups had lower endothelin-1 and creatinine concentrations than the SHR group; the SHR + HA group also had lower aspartate aminotransferase and uric acid levels than the SHR group did. We later recruited 23 participants with overweight and obesity, and they consumed 60 g of dehulled adlay daily for a six-week experimental period. At the end of the study, we observed a significant decrease in the group’s systolic blood pressure (SBP), and the change in SBP was even more evident in participants with high baseline SBP. In conclusion, our results suggested that daily intake of dehulled adlay had beneficial effects in blood-pressure management. Future studies may further clarify the possible underlying mechanisms for the consuming of dehulled adlay as a beneficial dietary approach for people at risk of hypertension.

scholarly journals The Gut Microbiota and Healthy Aging: A Mini-Review

Gerontology ◽  
2018 ◽  
Vol 64 (6) ◽  
pp. 513-520 ◽  
Author(s):  
Sangkyu Kim ◽  
S. Michal Jazwinski
Keyword(s):  
Gut Microbiota ◽  
Individual Variation ◽  
Gut Microbiome ◽  
Chronological Age ◽  
Low Grade ◽  
Beneficial Effects ◽  
Gut Dysbiosis ◽  
Age Related ◽  
Host Health ◽  
Nutrient Signaling

The gut microbiota shows a wide inter-individual variation, but its within-individual variation is relatively stable over time. A functional core microbiome, provided by abundant bacterial taxa, seems to be common to various human hosts regardless of their gender, geographic location, and age. With advancing chronological age, the gut microbiota becomes more diverse and variable. However, when measures of biological age are used with adjustment for chronological age, overall richness decreases, while a certain group of bacteria associated with frailty increases. This highlights the importance of considering biological or functional measures of aging. Studies using model organisms indicate that age-related gut dysbiosis may contribute to unhealthy aging and reduced longevity. The gut microbiome depends on the host nutrient signaling pathways for its beneficial effects on host health and lifespan, and gut dysbiosis disrupting the interdependence may diminish the beneficial effects or even have reverse effects. Gut dysbiosis can trigger the innate immune response and chronic low-grade inflammation, leading to many age-related degenerative pathologies and unhealthy aging. The gut microbiota communicates with the host through various biomolecules, nutrient signaling-independent pathways, and epigenetic mechanisms. Disturbance of these communications by age-related gut dysbiosis can affect the host health and lifespan. This may explain the impact of the gut microbiome on health and aging.

scholarly journals Spring mineral water-borne bacteria reshape gut microbiota profiles and confer health benefits

2018 ◽  
Author(s):  
YP Chen ◽  
LL Tan ◽  
DM Chen ◽  
Q Xu ◽  
JP Song ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Mineral Water ◽  
Chromosomal Dna ◽  
Local Resident ◽  
Mitochondrial Dysfunctions ◽  
Sulfate Reducing ◽  
Beneficial Effects ◽  
Gut Dysbiosis ◽  
Live Bacteria ◽  
Reducing Bacteria

BackgroundAlthough dietary patterns are recognized to affect health by interfering with gut microbiota homeostasis, whether live or dead bacteria-bearing spring mineral water (MW) would also exert beneficial effects on health upon curing gut dysbiosis remains unknown.ResultsDue to harboring live bacteria, the heated but unboiled MW from Bama, where centenarians are ubiquitously inhabited, reshapes the gut microbiota from a traveler-type to a local resident-type except for Prevotella. While chondroitin sulfate, a component occurring in livestock and poultry meats, increases the richness of sulfatase-secreting bacteria and sulfate-reducing bacteria, Bama MW dampens the overgrowth of those colon-thinning bacteria and hampers the overexpression of multiple genes responsible for anti-inflammation, anti-oxidation, anti-hypoxia, anti-mutagenesis, and anti-tumorigenesis.ConclusionsBama spring MW prevents the early-phase onset of breast cancer by curating gut dysbiosis. MW also compromises chromosomal DNA damage and ameliorate mitochondrial dysfunctions, implying it may extend lifespan.

scholarly journals ACE Inhibition Reduces Infarction in Normotensive but Not Hypertensive Rats: Correlation with Cortical ACE Activity

2010 ◽  
Vol 30 (8) ◽  
pp. 1520-1526 ◽  
Author(s):  
Michelle J Porritt ◽  
Michelle Chen ◽  
Sarah SJ Rewell ◽  
Rachael G Dean ◽  
Louise M Burrell ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Infarct Volume ◽  
Ace Inhibition ◽  
Artery Occlusion ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects ◽  
Wky Rats ◽  
Ace Activity ◽  
Wistar Kyoto

Angiotensin-converting enzyme (ACE) inhibition can reduce stroke risk by up to 43% in humans and reduce the associated disability, and hence understanding the mechanism of improvement is important. In animals and humans, these effects may be independent of the blood pressure-lowering effects of ACE inhibition. Normotensive (Wistar–Kyoto (WKY)) and hypertensive (spontaneously hypertensive rat (SHR)) animals were treated with the ACE inhibitors ramipril or lisinopril for 7 or 42 days before 2 hours of transient middle cerebral artery occlusion (MCAo). Blood pressure, serum ACE, and blood glucose levels were measured and stroke infarct volume was recorded 24 hours after stroke. Despite greater reductions in blood pressure, infarct size was not improved by ACE inhibition in hypertensive animals. Short-term ACE inhibition produced only a modest reduction in blood pressure, but WKY rats showed marked reductions in infarct volume. Long-term ACE inhibition had additional reductions in blood pressure; however, infarct volumes in WKY rats did not improve further but worsened. WKY rats differed from SHR in having marked cortical ACE activity that was highly sensitive to ACE inhibition. The beneficial effects of ACE inhibition on infarct volume in normotensive rats do not correlate with changes in blood pressure. However, WKY rats have ACE inhibitor-sensitive cortical ACE activity that is lacking in the SHR.

Abstract MP38: Identification Of A Gut Microbe That Attenuates The Blood Pressure Lowering Effect Of ACEi Quinapril

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Tao Yang ◽  
Xue Mei ◽  
Ethel Tackie-Yarboi ◽  
Jun Kyoung ◽  
Blair Mell ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Drug Resistance ◽  
Drug Metabolism ◽  
Gut Microbiota ◽  
Esterase Activity ◽  
Enzyme Inhibitor ◽  
Fecal Microbiota ◽  
Blood Pressure Lowering Effect ◽  
Spontaneously Hypertensive ◽  
Cecal Microbiota

Introduction: Treatment resistant hypertension (rHTN) is present in ~20% of all hypertensive patients. rHTN is critical in African American patients who experience early onset, severe outcomes, and weak responsiveness to angiotensin converting enzyme inhibitor (ACEi). The mechanism for drug resistance is unknown. Gut microbiota harbors biotransformative enzymes such as esterase, which may hydrolyze ACEis, reducing absorption. Our study was to identify microbe responsible for ACEi resistance. Methods: 16-week-old male Spontaneously Hypertensive Rats (SHR) were gavaged with (N=12) or without (N=6) Vancomycin, Meropenem, and Omeprazole (VMO) 50 mg/kg/day for five days to deplete the gut microbiota. A single 8mg/kg dose of quinapril was given to SHR and SHR+VMO before blood pressure (BP) recording via telemetry. Quinapril catabolism was quantified by liquid chromatography-mass spectrometry. Bacterial esterase activity was monitored by hydrolysis of p-nitro-phenylbutyrate. Cecal microbiota was analyzed by 16S rDNA. Fecal microbiota were analyzed by metagenomics in 29 (16 black, 13 white) HTN patients. Results: Quinapril lowered BP more in the SHR+VMO than SHR ( P <0.0001). With a 50% reduction in bacterial 16S copy numbers ( P <0.0001), the SHR+VMO group showed (1) reduced Coprococcus ( P <0.0001); (2) lower esterase activity per gram of cecal microbiota to hydrolyze quinapril ( P =0.0065); (3) a 50% lower reduction in quinapril quantity (nmol) after incubation with 1mg of cecal lysate for 3 hr ( P <0.0001); (4) decreased bacterial genes in KEGG drug metabolism pathway ( P <0.0001). The abundance of Coprococcus positively correlated with genes in drug metabolism ( P <0.0001). Importantly, co-administration of quinapril with C. comes, a species in Coprococcus genus, reduced the BP-lowering effects of quinapril in the SHR ( P <0.0001). Comparison of human microbiota demonstrated a higher abundance of C. comes in the black hypertensives (poor ACEi responder) than the white (ACEi responder) ( P =0.0167). Conclusion: We, for the first time, demonstrate a previously unrecognized role of gut microbes in reducing ACEi effectiveness. This serves a foundation for expanding clinical management of antihypertensive drug resistance via manipulation of gut microbiota.

Recent Advances in Probiotics as Live Biotherapeutics Against Gastrointestinal Diseases

2018 ◽  
Vol 24 (27) ◽  
pp. 3162-3171 ◽  
Author(s):  
Rohini Krishna Kota ◽  
Ranga Rao Ambati ◽  
Aswani Kumar Y.V.V. ◽  
Krupanidhi Srirama ◽  
Prakash Narayana Reddy
Keyword(s):  
Gut Microbiota ◽  
Global Economy ◽  
Gastrointestinal Diseases ◽  
Therapeutic Strategies ◽  
Emergency Department Visits ◽  
Microbiota Composition ◽  
Probiotic Supplementation ◽  
Beneficial Effects ◽  
Gut Dysbiosis ◽  
Gut Microbiota Composition

Background: Gastrointestinal (GI) diseases are a major cause of emergency department visits requiring hospitalizations leading to considerable burden on global economy. Several factors contribute to the onset of gastrointestinal diseases such as pathogens (parasites, bacteria, virus, toxins etc.), autoimmune disorders and severe inflammation of intestine. Objective: One common feature among all these diseases is the dysentery and alteration of gut microbiota composition (gut dysbiosis). Apart from conventional therapies such as antibiotics and ORS supplementation, gut microbiota modulation with probiotic supplementation has emerged as a successful and healthy alternative in mitigating GI diseases. In this review our goal is to discuss the causes of gastrointestinal diseases and the present state of various therapeutic strategies such as probiotics as live biotherapeutics and Fecal Microbial Transplants (FMT’s). Conclusion: Several reports and clinical trials point out to the beneficial effects of probiotics in modulating the gut microbiota and improving the side effects of gastrointestinal diseases. Live biotherapeutics and FMT’s could be suitable and successful alternatives to conventional therapies in mitigating the gastrointestinal pathogens.

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