Hypertrophic cardiomyopathy and dysregulation of cardiac energetics in a mouse model of biliary fibrosis

Cardiac dysfunction is a major cause of morbidity and mortality in patients with end‐stage liver disease; yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterati...

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Published inHepatology (Baltimore, Md.) Vol. 51; no. 6; pp. 2097 - 2107
Main Authors Desai, Moreshwar S., Shabier, Zainuer, Taylor, Michael, Lam, Fong, Thevananther, Sundararajah, Kosters, Astrid, Karpen, Saul J.
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.06.2010
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Abstract Cardiac dysfunction is a major cause of morbidity and mortality in patients with end‐stage liver disease; yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterations in signaling pathways engaged in cardiac energy metabolism and hypertrophy, augmented by direct effects of high circulating levels of bile acids. Biliary fibrosis was induced in male C57BL/6J mice by feeding a 0.1% 3,5‐diethoxycarbonyl‐1,4‐dihydroxychollidine (DDC) supplemented diet. After 3 weeks, mice underwent live imaging (dual energy x‐ray absorptiometry [DEXA] scanning, two‐dimensional echocardiography [2DE], electrocardiography, cardiac magnetic resonance imaging), exercise treadmill testing, and histological and biochemical analyses of livers and hearts. Compared with chow‐fed mice, DDC‐fed mice fatigued earlier on the treadmill, with reduced VO2. Marked changes were identified electrophysiologically (bradycardia and prolonged QT interval) and functionally (hyperdynamic left ventricular [LV] contractility along with increased LV thickness). Hearts of DDC‐fed mice showed hypertrophic signaling (activation of v‐akt murine thymoma viral oncogene/protein kinase B [AKT], inhibition of glycogen synthase kinase‐3β [GSK3β], a 20‐fold up‐regulation of β myosin heavy chain RNA and elevated Gsα/Giα ratio. Genes regulating cardiac fatty acid oxidation pathways were suppressed, along with a threefold increase in myocardial glycogen content. Treatment of mouse cardiomyocytes (which express the membrane bile acid receptor TGR5) with potent natural TGR5 agonists, taurochenodeoxycholic acid and lithocholic acid, activated AKT and inhibited GSK3β, similar to the changes seen in DDC‐fed mouse hearts. This provides support for a novel mechanism whereby circulating natural bile acids can induce signaling pathways in heart associated with hypertrophy. Conclusion: Three weeks of DDC feeding‐induced biliary fibrosis leads to multiple functional, metabolic, electrophysiological, and hypertrophic adaptations in the mouse heart, recapitulating some of the features of human cirrhotic cardiomyopathy. Hepatology 2010;51:2097–2107
AbstractList Cardiac dysfunction is a major cause of morbidity and mortality in patients with end-stage liver disease; yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterations in signaling pathways engaged in cardiac energy metabolism and hypertrophy, augmented by direct effects of high circulating levels of bile acids. Biliary fibrosis was induced in male C57BL/6J mice by feeding a 0.1% 3,5-diethoxycarbonyl-1,4-dihydroxychollidine (DDC) supplemented diet. After 3 weeks, mice underwent live imaging (dual energy x-ray absorptiometry [DEXA] scanning, two-dimensional echocardiography [2DE], electrocardiography, cardiac magnetic resonance imaging), exercise treadmill testing, and histological and biochemical analyses of livers and hearts. Compared with chow-fed mice, DDC-fed mice fatigued earlier on the treadmill, with reduced VO2. Marked changes were identified electrophysiologically (bradycardia and prolonged QT interval) and functionally (hyperdynamic left ventricular [LV] contractility along with increased LV thickness). Hearts of DDC-fed mice showed hypertrophic signaling (activation of v-akt murine thymoma viral oncogene/protein kinase B [AKT], inhibition of glycogen synthase kinase-3[beta] [GSK3[beta]], a 20-fold up-regulation of [beta] myosin heavy chain RNA and elevated Gs[alpha]/Gi[alpha] ratio. Genes regulating cardiac fatty acid oxidation pathways were suppressed, along with a threefold increase in myocardial glycogen content. Treatment of mouse cardiomyocytes (which express the membrane bile acid receptor TGR5) with potent natural TGR5 agonists, taurochenodeoxycholic acid and lithocholic acid, activated AKT and inhibited GSK3[beta], similar to the changes seen in DDC-fed mouse hearts. This provides support for a novel mechanism whereby circulating natural bile acids can induce signaling pathways in heart associated with hypertrophy. Conclusion: Three weeks of DDC feeding-induced biliary fibrosis leads to multiple functional, metabolic, electrophysiological, and hypertrophic adaptations in the mouse heart, recapitulating some of the features of human cirrhotic cardiomyopathy. Hepatology 2010;51:2097-2107
Cardiac dysfunction is a major cause of morbidity and mortality in patients with end-stage liver disease; yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterations in signaling pathways engaged in cardiac energy metabolism and hypertrophy, augmented by direct effects of high circulating levels of bile acids. Biliary fibrosis was induced in male C57BL/6J mice by feeding a 0.1% 3,5-diethoxycarbonyl-1,4-dihydroxychollidine (DDC) supplemented diet. After 3 weeks, mice underwent live imaging (dual energy x-ray absorptiometry [DEXA] scanning, two-dimensional echocardiography [2DE], electrocardiography, cardiac magnetic resonance imaging), exercise treadmill testing, and histological and biochemical analyses of livers and hearts. Compared with chow-fed mice, DDC-fed mice fatigued earlier on the treadmill, with reduced VO(2). Marked changes were identified electrophysiologically (bradycardia and prolonged QT interval) and functionally (hyperdynamic left ventricular [LV] contractility along with increased LV thickness). Hearts of DDC-fed mice showed hypertrophic signaling (activation of v-akt murine thymoma viral oncogene/protein kinase B [AKT], inhibition of glycogen synthase kinase-3beta [GSK3beta], a 20-fold up-regulation of beta myosin heavy chain RNA and elevated G(s)alpha/G(i)alpha ratio. Genes regulating cardiac fatty acid oxidation pathways were suppressed, along with a threefold increase in myocardial glycogen content. Treatment of mouse cardiomyocytes (which express the membrane bile acid receptor TGR5) with potent natural TGR5 agonists, taurochenodeoxycholic acid and lithocholic acid, activated AKT and inhibited GSK3beta, similar to the changes seen in DDC-fed mouse hearts. This provides support for a novel mechanism whereby circulating natural bile acids can induce signaling pathways in heart associated with hypertrophy. Three weeks of DDC feeding-induced biliary fibrosis leads to multiple functional, metabolic, electrophysiological, and hypertrophic adaptations in the mouse heart, recapitulating some of the features of human cirrhotic cardiomyopathy.
Cardiac dysfunction is a major cause of morbidity and mortality in patients with end-stage liver disease; yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterations in signaling pathways engaged in cardiac energy metabolism and hypertrophy, augmented by direct effects of high circulating levels of bile acids. Biliary fibrosis was induced in male C57BL/6J mice by feeding a 0.1% 3,5-diethoxycarbonyl-1,4-dihydroxychollidine (DDC) supplemented diet. After 3 weeks, mice underwent live imaging (dual energy x-ray absorptiometry [DEXA] scanning, two-dimensional echocardiography [2DE], electrocardiography, cardiac magnetic resonance imaging), exercise treadmill testing, and histological and biochemical analyses of livers and hearts. Compared with chow-fed mice, DDC-fed mice fatigued earlier on the treadmill, with reduced VO sub(2). Marked changes were identified electrophysiologically (bradycardia and prolonged QT interval) and functionally (hyperdynamic left ventricular [LV] contractility along with increased LV thickness). Hearts of DDC-fed mice showed hypertrophic signaling (activation of v-akt murine thymoma viral oncogene/protein kinase B [AKT], inhibition of glycogen synthase kinase-3 beta [GSK3 beta ], a 20-fold up-regulation of beta myosin heavy chain RNA and elevated G sub(s) alpha /G sub(i) alpha ratio. Genes regulating cardiac fatty acid oxidation pathways were suppressed, along with a threefold increase in myocardial glycogen content. Treatment of mouse cardiomyocytes (which express the membrane bile acid receptor TGR5) with potent natural TGR5 agonists, taurochenodeoxycholic acid and lithocholic acid, activated AKT and inhibited GSK3 beta , similar to the changes seen in DDC-fed mouse hearts. This provides support for a novel mechanism whereby circulating natural bile acids can induce signaling pathways in heart associated with hypertrophy. Conclusion: Three weeks of DDC feeding-induced biliary fibrosis leads to multiple functional, metabolic, electrophysiological, and hypertrophic adaptations in the mouse heart, recapitulating some of the features of human cirrhotic cardiomyopathy. Hepatology 2010; 51:2097-2107
Cardiac dysfunction is a major cause of morbidity and mortality in patients with end‐stage liver disease; yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterations in signaling pathways engaged in cardiac energy metabolism and hypertrophy, augmented by direct effects of high circulating levels of bile acids. Biliary fibrosis was induced in male C57BL/6J mice by feeding a 0.1% 3,5‐diethoxycarbonyl‐1,4‐dihydroxychollidine (DDC) supplemented diet. After 3 weeks, mice underwent live imaging (dual energy x‐ray absorptiometry [DEXA] scanning, two‐dimensional echocardiography [2DE], electrocardiography, cardiac magnetic resonance imaging), exercise treadmill testing, and histological and biochemical analyses of livers and hearts. Compared with chow‐fed mice, DDC‐fed mice fatigued earlier on the treadmill, with reduced VO2. Marked changes were identified electrophysiologically (bradycardia and prolonged QT interval) and functionally (hyperdynamic left ventricular [LV] contractility along with increased LV thickness). Hearts of DDC‐fed mice showed hypertrophic signaling (activation of v‐akt murine thymoma viral oncogene/protein kinase B [AKT], inhibition of glycogen synthase kinase‐3β [GSK3β], a 20‐fold up‐regulation of β myosin heavy chain RNA and elevated Gsα/Giα ratio. Genes regulating cardiac fatty acid oxidation pathways were suppressed, along with a threefold increase in myocardial glycogen content. Treatment of mouse cardiomyocytes (which express the membrane bile acid receptor TGR5) with potent natural TGR5 agonists, taurochenodeoxycholic acid and lithocholic acid, activated AKT and inhibited GSK3β, similar to the changes seen in DDC‐fed mouse hearts. This provides support for a novel mechanism whereby circulating natural bile acids can induce signaling pathways in heart associated with hypertrophy. Conclusion: Three weeks of DDC feeding‐induced biliary fibrosis leads to multiple functional, metabolic, electrophysiological, and hypertrophic adaptations in the mouse heart, recapitulating some of the features of human cirrhotic cardiomyopathy. Hepatology 2010;51:2097–2107
Cardiac dysfunction is a major cause of morbidity and mortality in patients with end-stage liver disease, yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterations in signaling pathways engaged in cardiac energy metabolism and hypertrophy, augmented by direct effects of high circulating levels of bile acids. Biliary fibrosis was induced in male C57BL/6J mice by feeding a 0.1% 3, 5-diethoxycarbonyl-1, 4-dihydroxychollidine (DDC) supplemented diet. After 3 weeks, mice underwent live imaging (DEXA scanning, 2DEcho, EKG, cardiac MRI), exercise treadmill testing and histological and biochemical analyses of livers and hearts. Compared to chow-fed mice, DDC-fed mice fatigued earlier on the treadmill, with reduced VO 2 . Marked changes were identified electrophysiologically (bradycardia and prolonged QTc) and functionally (hyperdynamic left ventricular (LV) contractility along with increased LV thickness). Hearts of DDC-fed mice showed hypertrophic signaling (activation of AKT, inhibition of GSK3β and a 20-fold upregulation of β myosin heavy chain RNA) and elevated G s α/G i α ratio. Genes regulating cardiac fatty acid oxidation pathways were suppressed, along with a 3-fold increase in myocardial glycogen content. Treatment of mouse cardiomyocytes (which express the membrane bile acid receptor TGR5) with potent natural TGR5 agonists, taurochenodeoxycholic acid and lithocholic acid, activated AKT and inhibited GSK3β, similar to the changes seen in DDC-fed mouse hearts. This provides support for a novel mechanism whereby circulating natural bile acids can induce signaling pathways in heart associated with hypertrophy. In conclusion, 3 weeks of DDC feeding-induced biliary fibrosis leads to multiple functional, metabolic, electrophysiological and hypertrophic adaptations in the mouse heart recapitulating some of the features of human cirrhotic cardiomyopathy.
Author Thevananther, Sundararajah
Desai, Moreshwar S.
Shabier, Zainuer
Kosters, Astrid
Karpen, Saul J.
Lam, Fong
Taylor, Michael
AuthorAffiliation 3 Texas Children’s Liver Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, 77030, USA
2 Section of Pediatric Cardiology, Baylor College of Medicine, Houston TX
1 Section of Pediatric Critical Care, Baylor College of Medicine, Houston TX
AuthorAffiliation_xml – name: 3 Texas Children’s Liver Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, 77030, USA
– name: 1 Section of Pediatric Critical Care, Baylor College of Medicine, Houston TX
– name: 2 Section of Pediatric Cardiology, Baylor College of Medicine, Houston TX
Author_xml – sequence: 1
  givenname: Moreshwar S.
  surname: Desai
  fullname: Desai, Moreshwar S.
– sequence: 2
  givenname: Zainuer
  surname: Shabier
  fullname: Shabier, Zainuer
– sequence: 3
  givenname: Michael
  surname: Taylor
  fullname: Taylor, Michael
– sequence: 4
  givenname: Fong
  surname: Lam
  fullname: Lam, Fong
– sequence: 5
  givenname: Sundararajah
  surname: Thevananther
  fullname: Thevananther, Sundararajah
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  surname: Kosters
  fullname: Kosters, Astrid
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  givenname: Saul J.
  surname: Karpen
  fullname: Karpen, Saul J.
  email: skarpen@bcm.tmc.edu
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ISSN 0270-9139
IngestDate Tue Sep 17 21:18:05 EDT 2024
Wed Dec 04 01:19:43 EST 2024
Thu Oct 10 17:05:55 EDT 2024
Fri Dec 06 06:40:31 EST 2024
Tue Aug 27 13:46:28 EDT 2024
Sun Oct 29 17:07:38 EDT 2023
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Issue 6
Keywords Heart
Biliary tract
Rodentia
Cardiovascular disease
Myocardial disease
Vertebrata
Mammalia
Mouse
Heart disease
Animal
Fibrosis
Gastroenterology
Hypertrophic cardiomyopathy
Models
Language English
License CC BY 4.0
LinkModel DirectLink
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Notes Potential conflict of interest: Nothing to report.
fax: 832‐825‐4893
A portion of this work was presented in abstract form at the annual meeting of the AASLD, November 2009.
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Snippet Cardiac dysfunction is a major cause of morbidity and mortality in patients with end‐stage liver disease; yet the mechanisms remain largely unknown. We...
Cardiac dysfunction is a major cause of morbidity and mortality in patients with end-stage liver disease; yet the mechanisms remain largely unknown. We...
Cardiac dysfunction is a major cause of morbidity and mortality in patients with end-stage liver disease, yet the mechanisms remain largely unknown. We...
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StartPage 2097
SubjectTerms Animals
Bile
Bile Acids and Salts - blood
Bile Duct Diseases - chemically induced
Bile Duct Diseases - complications
Bile Duct Diseases - metabolism
Bile Duct Diseases - physiopathology
Biological and medical sciences
Cardiology. Vascular system
Cardiomyopathy
Cardiomyopathy, Hypertrophic - etiology
Dicarbethoxydihydrocollidine
Disease Models, Animal
Fatigue - chemically induced
Fatigue - complications
Fatty Acids - metabolism
Fibrosis
Fitness equipment
Gastroenterology. Liver. Pancreas. Abdomen
Gene Expression - drug effects
Glycogen - metabolism
Heart
Heart - physiopathology
Hepatology
Kinases
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
Mice
Mice, Inbred C57BL
Mortality
Myocarditis. Cardiomyopathies
Myocardium - metabolism
Myocardium - pathology
Oxygen Consumption
Phenotype
Receptors, Adrenergic, beta - metabolism
Receptors, G-Protein-Coupled - metabolism
Respiratory Function Tests
Rodents
Signal Transduction
Title Hypertrophic cardiomyopathy and dysregulation of cardiac energetics in a mouse model of biliary fibrosis
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fhep.23585
https://www.ncbi.nlm.nih.gov/pubmed/20512997
https://www.proquest.com/docview/1766822482
https://search.proquest.com/docview/1776669805
https://pubmed.ncbi.nlm.nih.gov/PMC3678910
Volume 51
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