Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure

Francine Coelho Marques, Erin M. Nelson, Po Yin Chu, Duncan Horlock, April Fiedler, Mark Daniel Ziemann, Jian Tan, Don Monath Sanjaya Kuruppu, Niwanthi Rajapakse, Assam El-Osta, Charles R. Mackay, David Martin Kaye

Research output: Contribution to conferenceAbstractOther

Abstract

Introduction: Although dietary intake of fruit and vegetables is associated with lower incidence of cardiovascular disease, the mechanism involved is not clear. Consumption of a diet high in fibre increases gut microbiota populations that generate short chain fatty acids (SCFAs) such as acetate, which has a protective role in experimental models of inflammatory diseases. Hypothesis: We hypothesised that SCFAs, including acetate, would attenuate the development of cardiac fibrosis in a mineralocorticoid-excess (MRE) model, given that inflammation has also been implicated in cardiac remodelling. Methods: Mice were fed control chow (47.6% fibre), high fibre chow (72.7% fibre) or water supplemented with acetate for 3 weeks, and then submitted to sham (uninephrectomy+1% salt) or MRE (uninephrectomy+1% salt+ DOCA tablet) surgeries (n=11-14/group). At the end of 6 weeks, cardiac structure (cardiac weight index and fibrosis by Mason trychrome) and function (by echocardiography) were examined. The gut microbiota was determined by next-generation sequencing of the 16S gene, and RNA-sequencing established the mechanisms involved. Results: Compared to MRE mice fed a normal diet, those fed a high fibre diet or acetate had significantly less cardiac hypertrophy, perivascular and interstitial cardiac fibrosis, and improved cardiac function (all P<0.05). Mice fed a high fibre diet or acetate had a profound effect on the activity circadian clock genes and decreased TGF-β and immune response. The protective effects of high fibre and acetate were accompanied by a decrease in the ratio of bacteria from the phylum Firmicutes compared to Bacteroidetes in both sham and DOCA groups (0.56 control vs 0.14 fibre vs 0.18 acetate, P=0.0005). Conclusions: Our study supports that dietary high fibre intake, through the SCFA acetate, can prevent heart failure by reducing cardiac fibrosis and improving cardiac function during MRE. This was accompanied by changes in the gut microbiota, supporting a gut-heart connection in the prevention of heart disease.
Original languageEnglish
Number of pages1
Publication statusPublished - 11 Nov 2016
EventAmerican-Heart-Association Scientific Sessions - New Orleans, United States of America
Duration: 12 Nov 201616 Dec 2016

Conference

ConferenceAmerican-Heart-Association Scientific Sessions
CountryUnited States of America
CityNew Orleans
Period12/11/1616/12/16

Cite this

Coelho Marques, F., Nelson, E. M., Chu, P. Y., Horlock, D., Fiedler, A., Ziemann, M. D., ... Kaye, D. M. (2016). Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure. Abstract from American-Heart-Association Scientific Sessions , New Orleans, United States of America.
Coelho Marques, Francine ; Nelson, Erin M. ; Chu, Po Yin ; Horlock, Duncan ; Fiedler, April ; Ziemann, Mark Daniel ; Tan, Jian ; Kuruppu, Don Monath Sanjaya ; Rajapakse, Niwanthi ; El-Osta, Assam ; Mackay, Charles R. ; Kaye, David Martin. / Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure. Abstract from American-Heart-Association Scientific Sessions , New Orleans, United States of America.1 p.
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title = "Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure",
abstract = "Introduction: Although dietary intake of fruit and vegetables is associated with lower incidence of cardiovascular disease, the mechanism involved is not clear. Consumption of a diet high in fibre increases gut microbiota populations that generate short chain fatty acids (SCFAs) such as acetate, which has a protective role in experimental models of inflammatory diseases. Hypothesis: We hypothesised that SCFAs, including acetate, would attenuate the development of cardiac fibrosis in a mineralocorticoid-excess (MRE) model, given that inflammation has also been implicated in cardiac remodelling. Methods: Mice were fed control chow (47.6{\%} fibre), high fibre chow (72.7{\%} fibre) or water supplemented with acetate for 3 weeks, and then submitted to sham (uninephrectomy+1{\%} salt) or MRE (uninephrectomy+1{\%} salt+ DOCA tablet) surgeries (n=11-14/group). At the end of 6 weeks, cardiac structure (cardiac weight index and fibrosis by Mason trychrome) and function (by echocardiography) were examined. The gut microbiota was determined by next-generation sequencing of the 16S gene, and RNA-sequencing established the mechanisms involved. Results: Compared to MRE mice fed a normal diet, those fed a high fibre diet or acetate had significantly less cardiac hypertrophy, perivascular and interstitial cardiac fibrosis, and improved cardiac function (all P<0.05). Mice fed a high fibre diet or acetate had a profound effect on the activity circadian clock genes and decreased TGF-β and immune response. The protective effects of high fibre and acetate were accompanied by a decrease in the ratio of bacteria from the phylum Firmicutes compared to Bacteroidetes in both sham and DOCA groups (0.56 control vs 0.14 fibre vs 0.18 acetate, P=0.0005). Conclusions: Our study supports that dietary high fibre intake, through the SCFA acetate, can prevent heart failure by reducing cardiac fibrosis and improving cardiac function during MRE. This was accompanied by changes in the gut microbiota, supporting a gut-heart connection in the prevention of heart disease.",
author = "{Coelho Marques}, Francine and Nelson, {Erin M.} and Chu, {Po Yin} and Duncan Horlock and April Fiedler and Ziemann, {Mark Daniel} and Jian Tan and Kuruppu, {Don Monath Sanjaya} and Niwanthi Rajapakse and Assam El-Osta and Mackay, {Charles R.} and Kaye, {David Martin}",
year = "2016",
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note = "American-Heart-Association Scientific Sessions ; Conference date: 12-11-2016 Through 16-12-2016",

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Coelho Marques, F, Nelson, EM, Chu, PY, Horlock, D, Fiedler, A, Ziemann, MD, Tan, J, Kuruppu, DMS, Rajapakse, N, El-Osta, A, Mackay, CR & Kaye, DM 2016, 'Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure' American-Heart-Association Scientific Sessions , New Orleans, United States of America, 12/11/16 - 16/12/16, .

Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure. / Coelho Marques, Francine; Nelson, Erin M.; Chu, Po Yin; Horlock, Duncan; Fiedler, April; Ziemann, Mark Daniel; Tan, Jian; Kuruppu, Don Monath Sanjaya; Rajapakse, Niwanthi; El-Osta, Assam; Mackay, Charles R.; Kaye, David Martin.

2016. Abstract from American-Heart-Association Scientific Sessions , New Orleans, United States of America.

Research output: Contribution to conferenceAbstractOther

TY - CONF

T1 - Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure

AU - Coelho Marques, Francine

AU - Nelson, Erin M.

AU - Chu, Po Yin

AU - Horlock, Duncan

AU - Fiedler, April

AU - Ziemann, Mark Daniel

AU - Tan, Jian

AU - Kuruppu, Don Monath Sanjaya

AU - Rajapakse, Niwanthi

AU - El-Osta, Assam

AU - Mackay, Charles R.

AU - Kaye, David Martin

PY - 2016/11/11

Y1 - 2016/11/11

N2 - Introduction: Although dietary intake of fruit and vegetables is associated with lower incidence of cardiovascular disease, the mechanism involved is not clear. Consumption of a diet high in fibre increases gut microbiota populations that generate short chain fatty acids (SCFAs) such as acetate, which has a protective role in experimental models of inflammatory diseases. Hypothesis: We hypothesised that SCFAs, including acetate, would attenuate the development of cardiac fibrosis in a mineralocorticoid-excess (MRE) model, given that inflammation has also been implicated in cardiac remodelling. Methods: Mice were fed control chow (47.6% fibre), high fibre chow (72.7% fibre) or water supplemented with acetate for 3 weeks, and then submitted to sham (uninephrectomy+1% salt) or MRE (uninephrectomy+1% salt+ DOCA tablet) surgeries (n=11-14/group). At the end of 6 weeks, cardiac structure (cardiac weight index and fibrosis by Mason trychrome) and function (by echocardiography) were examined. The gut microbiota was determined by next-generation sequencing of the 16S gene, and RNA-sequencing established the mechanisms involved. Results: Compared to MRE mice fed a normal diet, those fed a high fibre diet or acetate had significantly less cardiac hypertrophy, perivascular and interstitial cardiac fibrosis, and improved cardiac function (all P<0.05). Mice fed a high fibre diet or acetate had a profound effect on the activity circadian clock genes and decreased TGF-β and immune response. The protective effects of high fibre and acetate were accompanied by a decrease in the ratio of bacteria from the phylum Firmicutes compared to Bacteroidetes in both sham and DOCA groups (0.56 control vs 0.14 fibre vs 0.18 acetate, P=0.0005). Conclusions: Our study supports that dietary high fibre intake, through the SCFA acetate, can prevent heart failure by reducing cardiac fibrosis and improving cardiac function during MRE. This was accompanied by changes in the gut microbiota, supporting a gut-heart connection in the prevention of heart disease.

AB - Introduction: Although dietary intake of fruit and vegetables is associated with lower incidence of cardiovascular disease, the mechanism involved is not clear. Consumption of a diet high in fibre increases gut microbiota populations that generate short chain fatty acids (SCFAs) such as acetate, which has a protective role in experimental models of inflammatory diseases. Hypothesis: We hypothesised that SCFAs, including acetate, would attenuate the development of cardiac fibrosis in a mineralocorticoid-excess (MRE) model, given that inflammation has also been implicated in cardiac remodelling. Methods: Mice were fed control chow (47.6% fibre), high fibre chow (72.7% fibre) or water supplemented with acetate for 3 weeks, and then submitted to sham (uninephrectomy+1% salt) or MRE (uninephrectomy+1% salt+ DOCA tablet) surgeries (n=11-14/group). At the end of 6 weeks, cardiac structure (cardiac weight index and fibrosis by Mason trychrome) and function (by echocardiography) were examined. The gut microbiota was determined by next-generation sequencing of the 16S gene, and RNA-sequencing established the mechanisms involved. Results: Compared to MRE mice fed a normal diet, those fed a high fibre diet or acetate had significantly less cardiac hypertrophy, perivascular and interstitial cardiac fibrosis, and improved cardiac function (all P<0.05). Mice fed a high fibre diet or acetate had a profound effect on the activity circadian clock genes and decreased TGF-β and immune response. The protective effects of high fibre and acetate were accompanied by a decrease in the ratio of bacteria from the phylum Firmicutes compared to Bacteroidetes in both sham and DOCA groups (0.56 control vs 0.14 fibre vs 0.18 acetate, P=0.0005). Conclusions: Our study supports that dietary high fibre intake, through the SCFA acetate, can prevent heart failure by reducing cardiac fibrosis and improving cardiac function during MRE. This was accompanied by changes in the gut microbiota, supporting a gut-heart connection in the prevention of heart disease.

UR - https://www.ahajournals.org/doi/10.1161/circ.134.suppl_1.18617

M3 - Abstract

ER -

Coelho Marques F, Nelson EM, Chu PY, Horlock D, Fiedler A, Ziemann MD et al. Effect of Dietary Fibre Intake and the Gut Microbiota in a Model of Heart Failure. 2016. Abstract from American-Heart-Association Scientific Sessions , New Orleans, United States of America.