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Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models

BACKGROUND: Pathophysiological processes underlying diabetic-related cardiomyopathies are complex. Mitochondria dysfunction is often described as a cause of cardiac impairment but its extent may depend on the type of experimental diabetes. Here we proposed to compare drug- or diet-induced models of...

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Autores principales: Marciniak, Camille, Marechal, Xavier, Montaigne, David, Neviere, Remi, Lancel, Steve
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4243842/
https://www.ncbi.nlm.nih.gov/pubmed/25142225
http://dx.doi.org/10.1186/s12933-014-0118-7
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author Marciniak, Camille
Marechal, Xavier
Montaigne, David
Neviere, Remi
Lancel, Steve
author_facet Marciniak, Camille
Marechal, Xavier
Montaigne, David
Neviere, Remi
Lancel, Steve
author_sort Marciniak, Camille
collection PubMed
description BACKGROUND: Pathophysiological processes underlying diabetic-related cardiomyopathies are complex. Mitochondria dysfunction is often described as a cause of cardiac impairment but its extent may depend on the type of experimental diabetes. Here we proposed to compare drug- or diet-induced models of diabetes in terms of metabolic features, cardiac and mitochondrial functions. METHODS: Mice were fed with regular chow or fat-enriched diet. After three weeks, they received either citrate or streptozotocin injections for five consecutive days. Metabolic parameters, myocardial contractile function and mitochondrial respiration were measured after three more weeks. Fat mass volumes were assessed by magnetic resonance imaging. Oral glucose tolerance test, insulin tolerance test, triglyceride and adipocytokine quantification were evaluated to establish metabolic profiles. Cardiac function was assessed ex vivo onto a Langendorff column. Isolated cardiac mitochondria respiration was obtained using high-resolution oxygraphy. RESULTS: Mice fed with the fat-enriched regimen presented abdominal obesity, increased blood glucose, elevated leptin level, glucose intolerance, and insulin resistance. Mice treated with streptozotocin, independently of the regimen, lost their capacity to release insulin in response to glucose ingestion. Mice fed with regular chow diet and injected with streptozotocin developed cardiac dysfunction without mitochondrial respiration defect. However, both groups of high-fat diet fed mice developed cardiac alterations associated with reduction in mitochondrial oxygen consumption, despite an increase in mitochondrial biogenesis signalling. CONCLUSIONS: We explored three animal models mimicking type 1 and 2 diabetes. While cardiac dysfunction was present in the three groups of mice, mitochondrial respiration impairment was only obvious in models reproducing features of type 2 diabetes.
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spelling pubmed-42438422014-11-26 Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models Marciniak, Camille Marechal, Xavier Montaigne, David Neviere, Remi Lancel, Steve Cardiovasc Diabetol Original Investigation BACKGROUND: Pathophysiological processes underlying diabetic-related cardiomyopathies are complex. Mitochondria dysfunction is often described as a cause of cardiac impairment but its extent may depend on the type of experimental diabetes. Here we proposed to compare drug- or diet-induced models of diabetes in terms of metabolic features, cardiac and mitochondrial functions. METHODS: Mice were fed with regular chow or fat-enriched diet. After three weeks, they received either citrate or streptozotocin injections for five consecutive days. Metabolic parameters, myocardial contractile function and mitochondrial respiration were measured after three more weeks. Fat mass volumes were assessed by magnetic resonance imaging. Oral glucose tolerance test, insulin tolerance test, triglyceride and adipocytokine quantification were evaluated to establish metabolic profiles. Cardiac function was assessed ex vivo onto a Langendorff column. Isolated cardiac mitochondria respiration was obtained using high-resolution oxygraphy. RESULTS: Mice fed with the fat-enriched regimen presented abdominal obesity, increased blood glucose, elevated leptin level, glucose intolerance, and insulin resistance. Mice treated with streptozotocin, independently of the regimen, lost their capacity to release insulin in response to glucose ingestion. Mice fed with regular chow diet and injected with streptozotocin developed cardiac dysfunction without mitochondrial respiration defect. However, both groups of high-fat diet fed mice developed cardiac alterations associated with reduction in mitochondrial oxygen consumption, despite an increase in mitochondrial biogenesis signalling. CONCLUSIONS: We explored three animal models mimicking type 1 and 2 diabetes. While cardiac dysfunction was present in the three groups of mice, mitochondrial respiration impairment was only obvious in models reproducing features of type 2 diabetes. BioMed Central 2014-08-21 /pmc/articles/PMC4243842/ /pubmed/25142225 http://dx.doi.org/10.1186/s12933-014-0118-7 Text en © Marciniak et al.; licensee BioMed Central Ltd. 2014 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Original Investigation
Marciniak, Camille
Marechal, Xavier
Montaigne, David
Neviere, Remi
Lancel, Steve
Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models
title Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models
title_full Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models
title_fullStr Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models
title_full_unstemmed Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models
title_short Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models
title_sort cardiac contractile function and mitochondrial respiration in diabetes-related mouse models
topic Original Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4243842/
https://www.ncbi.nlm.nih.gov/pubmed/25142225
http://dx.doi.org/10.1186/s12933-014-0118-7
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