Heart failure developed after myocardial infarction does not affect gut microbiota composition in the rat

There is a body of evidence that supports the notion that gut dysbiosis plays a role in the pathogenesis of cardiovascular diseases. Decreased cardiac function can reduce intestinal perfusion, resulting in morphological alterations, which may contribute to changes in the gut microbiota composition i...

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Veröffentlicht in:American journal of physiology: Gastrointestinal and liver physiology 2019-09, Vol.317 (3), p.G342-G348
Hauptverfasser: Lataro, Renata M, Imori, Priscilla F M, Santos, Emerson S, Silva, Luiz Eduardo V, Duarte, Rubens T D, Silva, Carlos A A, Falcão, Juliana P, Paton, Julian F R, Salgado, Helio C
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container_end_page G348
container_issue 3
container_start_page G342
container_title American journal of physiology: Gastrointestinal and liver physiology
container_volume 317
creator Lataro, Renata M
Imori, Priscilla F M
Santos, Emerson S
Silva, Luiz Eduardo V
Duarte, Rubens T D
Silva, Carlos A A
Falcão, Juliana P
Paton, Julian F R
Salgado, Helio C
description There is a body of evidence that supports the notion that gut dysbiosis plays a role in the pathogenesis of cardiovascular diseases. Decreased cardiac function can reduce intestinal perfusion, resulting in morphological alterations, which may contribute to changes in the gut microbiota composition in patients with heart failure (HF). In this regard, a germane question is whether changes in gut microbiota composition are a cause or consequence of the cardiovascular disturbance. We tested the hypothesis that the development of HF, after myocardial infarction, would cause gut dysbiosis. Fecal samples were collected before and 6 wk after myocardial infarction or sham surgery. Gut microbiota were characterized by sequencing the bacterial 16S ribosomal DNA. The composition of bacterial communities in the fecal samples was evaluated by calculating three major ecological parameters: ) the Chao 1 richness, ) the Pielou evenness, and ) the Shannon index. None of these indices was changed in either sham or HF rats. The ratio was not altered in HF rats. The number of species in each phylum was also not different between sham and HF rats. β-Diversity analysis showed that the composition of gut microbiota was not changed with the development of HF. Bacterial genera were grouped according to their major metabolic end-products (acetate, butyrate, and lactate), but no differences were observed in HF rats. Therefore, we conclude that HF induced by myocardial infarction does not affect gut microbiota composition, at least in rats, indicating that the dysbiosis observed in patients with HF may precede cardiovascular disturbance. Our study demonstrated that, following myocardial infarction in rats, heart failure (HF) development did not affect the intestinal microbiota despite distinct differences reported in the gut microbiota of humans with HF. Our finding is consistent with the notion that dysbiosis observed in patients with HF may precede cardiovascular dysfunction and therefore offers potential for early diagnosis and treatment.
doi_str_mv 10.1152/ajpgi.00018.2019
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Decreased cardiac function can reduce intestinal perfusion, resulting in morphological alterations, which may contribute to changes in the gut microbiota composition in patients with heart failure (HF). In this regard, a germane question is whether changes in gut microbiota composition are a cause or consequence of the cardiovascular disturbance. We tested the hypothesis that the development of HF, after myocardial infarction, would cause gut dysbiosis. Fecal samples were collected before and 6 wk after myocardial infarction or sham surgery. Gut microbiota were characterized by sequencing the bacterial 16S ribosomal DNA. The composition of bacterial communities in the fecal samples was evaluated by calculating three major ecological parameters: ) the Chao 1 richness, ) the Pielou evenness, and ) the Shannon index. None of these indices was changed in either sham or HF rats. The ratio was not altered in HF rats. The number of species in each phylum was also not different between sham and HF rats. β-Diversity analysis showed that the composition of gut microbiota was not changed with the development of HF. Bacterial genera were grouped according to their major metabolic end-products (acetate, butyrate, and lactate), but no differences were observed in HF rats. Therefore, we conclude that HF induced by myocardial infarction does not affect gut microbiota composition, at least in rats, indicating that the dysbiosis observed in patients with HF may precede cardiovascular disturbance. Our study demonstrated that, following myocardial infarction in rats, heart failure (HF) development did not affect the intestinal microbiota despite distinct differences reported in the gut microbiota of humans with HF. 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Decreased cardiac function can reduce intestinal perfusion, resulting in morphological alterations, which may contribute to changes in the gut microbiota composition in patients with heart failure (HF). In this regard, a germane question is whether changes in gut microbiota composition are a cause or consequence of the cardiovascular disturbance. We tested the hypothesis that the development of HF, after myocardial infarction, would cause gut dysbiosis. Fecal samples were collected before and 6 wk after myocardial infarction or sham surgery. Gut microbiota were characterized by sequencing the bacterial 16S ribosomal DNA. The composition of bacterial communities in the fecal samples was evaluated by calculating three major ecological parameters: ) the Chao 1 richness, ) the Pielou evenness, and ) the Shannon index. None of these indices was changed in either sham or HF rats. The ratio was not altered in HF rats. The number of species in each phylum was also not different between sham and HF rats. β-Diversity analysis showed that the composition of gut microbiota was not changed with the development of HF. Bacterial genera were grouped according to their major metabolic end-products (acetate, butyrate, and lactate), but no differences were observed in HF rats. Therefore, we conclude that HF induced by myocardial infarction does not affect gut microbiota composition, at least in rats, indicating that the dysbiosis observed in patients with HF may precede cardiovascular disturbance. Our study demonstrated that, following myocardial infarction in rats, heart failure (HF) development did not affect the intestinal microbiota despite distinct differences reported in the gut microbiota of humans with HF. Our finding is consistent with the notion that dysbiosis observed in patients with HF may precede cardiovascular dysfunction and therefore offers potential for early diagnosis and treatment.</description><subject>Acetic acid</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Cardiovascular diseases</subject><subject>Congestive heart failure</subject><subject>Coronary artery disease</subject><subject>Digestive system</subject><subject>DNA sequencing</subject><subject>Dysbacteriosis</subject><subject>Dysbiosis - microbiology</subject><subject>Feces - microbiology</subject><subject>Gastrointestinal Microbiome - genetics</subject><subject>Gastrointestinal tract</subject><subject>Heart attacks</subject><subject>Heart failure</subject><subject>Heart Failure - complications</subject><subject>Heart Failure - physiopathology</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Intestines - microbiology</subject><subject>Intestines - pathology</subject><subject>Lactic acid</subject><subject>Male</subject><subject>Microbiota</subject><subject>Microbiota - drug effects</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - microbiology</subject><subject>Perfusion</subject><subject>Rats, Wistar</subject><subject>Ribosomal DNA</subject><subject>Surgery</subject><issn>0193-1857</issn><issn>1522-1547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kMFLwzAUh4Mobk7vniTgubMvabrmKEOdMPCi55ImLzNjbWqaCvvvzTb19ODH99778RFyC_kcQLAHte03bp7nOVRzloM8I9MUswxEsTgn05TwDCqxmJCrYdgmTjCASzLhwKEQRTUlboUqRGqV240BqcFv3PkeDVU2YqDt3msVjFM76jqrgo7Od9R4HGjnY4Is6kg3Y6St08E3zkdFtW97P7gj6joaP5EGFa_JhVW7AW9-54x8PD-9L1fZ-u3ldfm4zjQvZUx1OTNqoRBMJbiWpWHcWmUbgASgMYyVUjAurayMVBaYRiZsLkA3rBTIZ-T-dLcP_mvEIdZbP4YuvawZq7gUXBZVovITlVoPQ0Bb98G1KuxryOuD2_rotj66rQ9u08rd7-GxadH8L_zJ5D8a8XdD</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Lataro, Renata M</creator><creator>Imori, Priscilla F M</creator><creator>Santos, Emerson S</creator><creator>Silva, Luiz Eduardo V</creator><creator>Duarte, Rubens T D</creator><creator>Silva, Carlos A A</creator><creator>Falcão, Juliana P</creator><creator>Paton, Julian F R</creator><creator>Salgado, Helio C</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><orcidid>https://orcid.org/0000-0002-9183-3926</orcidid></search><sort><creationdate>20190901</creationdate><title>Heart failure developed after myocardial infarction does not affect gut microbiota composition in the rat</title><author>Lataro, Renata M ; 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The number of species in each phylum was also not different between sham and HF rats. β-Diversity analysis showed that the composition of gut microbiota was not changed with the development of HF. Bacterial genera were grouped according to their major metabolic end-products (acetate, butyrate, and lactate), but no differences were observed in HF rats. Therefore, we conclude that HF induced by myocardial infarction does not affect gut microbiota composition, at least in rats, indicating that the dysbiosis observed in patients with HF may precede cardiovascular disturbance. Our study demonstrated that, following myocardial infarction in rats, heart failure (HF) development did not affect the intestinal microbiota despite distinct differences reported in the gut microbiota of humans with HF. Our finding is consistent with the notion that dysbiosis observed in patients with HF may precede cardiovascular dysfunction and therefore offers potential for early diagnosis and treatment.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>31314548</pmid><doi>10.1152/ajpgi.00018.2019</doi><orcidid>https://orcid.org/0000-0002-9183-3926</orcidid><oa>free_for_read</oa></addata></record>
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subjects Acetic acid
Animals
Bacteria
Cardiovascular diseases
Congestive heart failure
Coronary artery disease
Digestive system
DNA sequencing
Dysbacteriosis
Dysbiosis - microbiology
Feces - microbiology
Gastrointestinal Microbiome - genetics
Gastrointestinal tract
Heart attacks
Heart failure
Heart Failure - complications
Heart Failure - physiopathology
Intestinal microflora
Intestine
Intestines - microbiology
Intestines - pathology
Lactic acid
Male
Microbiota
Microbiota - drug effects
Myocardial infarction
Myocardial Infarction - microbiology
Perfusion
Rats, Wistar
Ribosomal DNA
Surgery
title Heart failure developed after myocardial infarction does not affect gut microbiota composition in the rat
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