Altered mitochondrial metabolism in the insulin‐resistant heart

Obesity‐induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this case, cardiac dysfunction is characterized by metabolic disturbances such as impaired glucose oxidation and an increased reliance on fatty acid (...

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Published inActa Physiologica Vol. 228; no. 3; pp. e13430 - n/a
Main Authors Makrecka‐Kuka, Marina, Liepinsh, Edgars, Murray, Andrew J., Lemieux, Hélène, Dambrova, Maija, Tepp, Kersti, Puurand, Marju, Käämbre, Tuuli, Han, Woo H., Goede, Paul, O'Brien, Katie A., Turan, Belma, Tuncay, Erkan, Olgar, Yusuf, Rolo, Anabela P., Palmeira, Carlos M., Boardman, Neoma T., Wüst, Rob C. I., Larsen, Terje S.
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.03.2020
Wiley
Subjects
Bioenergetics
Cardiomyopathy
Diabetes
Diabetes mellitus (non-insulin dependent)
heart
Insulin
Insulin resistance
lipotoxicity
Medical disciplines: 700
Medisinske Fag: 700
Metabolism
Mitochondria
Non-pharmacological intervention
Oxidation
Oxidative phosphorylation
Phosphorylation
VDP
diabetes
mitochondria
heart
lipotoxicity
Online AccessGet full text
ISSN1748-1708
1748-1716
1748-1716
DOI10.1111/apha.13430

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Abstract Obesity‐induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this case, cardiac dysfunction is characterized by metabolic disturbances such as impaired glucose oxidation and an increased reliance on fatty acid (FA) oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from FA‐induced lipotoxicity and uncoupling of oxidative phosphorylation. In this review, we address the metabolic changes in the diabetic heart, focusing on the loss of metabolic flexibility and cardiac mitochondrial function. We consider the alterations observed in mitochondrial substrate utilization, bioenergetics and dynamics, and highlight new areas of research which may improve our understanding of the cause and effect of cardiac mitochondrial dysfunction in diabetes. Finally, we explore how lifestyle (nutrition and exercise) and pharmacological interventions can prevent and treat metabolic and mitochondrial dysfunction in diabetes.
AbstractList Obesity‐induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this case, cardiac dysfunction is characterized by metabolic disturbances such as impaired glucose oxidation and an increased reliance on fatty acid (FA) oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from FA‐induced lipotoxicity and uncoupling of oxidative phosphorylation. In this review, we address the metabolic changes in the diabetic heart, focusing on the loss of metabolic flexibility and cardiac mitochondrial function. We consider the alterations observed in mitochondrial substrate utilization, bioenergetics and dynamics, and highlight new areas of research which may improve our understanding of the cause and effect of cardiac mitochondrial dysfunction in diabetes. Finally, we explore how lifestyle (nutrition and exercise) and pharmacological interventions can prevent and treat metabolic and mitochondrial dysfunction in diabetes.
Obesity-induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this case, cardiac dysfunction is characterized by metabolic disturbances such as impaired glucose oxidation and an increased reliance on fatty acid (FA) oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from FA-induced lipotoxicity and uncoupling of oxidative phosphorylation. In this review, we address the metabolic changes in the diabetic heart, focusing on the loss of metabolic flexibility and cardiac mitochondrial function. We consider the alterations observed in mitochondrial substrate utilization, bioenergetics and dynamics, and highlight new areas of research which may improve our understanding of the cause and effect of cardiac mitochondrial dysfunction in diabetes. Finally, we explore how lifestyle (nutrition and exercise) and pharmacological interventions can prevent and treat metabolic and mitochondrial dysfunction in diabetes.Obesity-induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this case, cardiac dysfunction is characterized by metabolic disturbances such as impaired glucose oxidation and an increased reliance on fatty acid (FA) oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from FA-induced lipotoxicity and uncoupling of oxidative phosphorylation. In this review, we address the metabolic changes in the diabetic heart, focusing on the loss of metabolic flexibility and cardiac mitochondrial function. We consider the alterations observed in mitochondrial substrate utilization, bioenergetics and dynamics, and highlight new areas of research which may improve our understanding of the cause and effect of cardiac mitochondrial dysfunction in diabetes. Finally, we explore how lifestyle (nutrition and exercise) and pharmacological interventions can prevent and treat metabolic and mitochondrial dysfunction in diabetes.
Author Olgar, Yusuf
Puurand, Marju
Boardman, Neoma T.
Liepinsh, Edgars
Tepp, Kersti
Wüst, Rob C. I.
Tuncay, Erkan
O'Brien, Katie A.
Larsen, Terje S.
Murray, Andrew J.
Lemieux, Hélène
Rolo, Anabela P.
Goede, Paul
Han, Woo H.
Turan, Belma
Palmeira, Carlos M.
Käämbre, Tuuli
Makrecka‐Kuka, Marina
Dambrova, Maija
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  fullname: Makrecka‐Kuka, Marina
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  organization: University of Amsterdam
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  givenname: Katie A.
  surname: O'Brien
  fullname: O'Brien, Katie A.
  organization: University of Cambridge
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  givenname: Belma
  surname: Turan
  fullname: Turan, Belma
  organization: University of Amsterdam
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  givenname: Erkan
  surname: Tuncay
  fullname: Tuncay, Erkan
  organization: Ankara University
– sequence: 14
  givenname: Yusuf
  surname: Olgar
  fullname: Olgar, Yusuf
  organization: Ankara University
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  givenname: Anabela P.
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  fullname: Rolo, Anabela P.
  organization: University of Coimbra
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  givenname: Carlos M.
  surname: Palmeira
  fullname: Palmeira, Carlos M.
  organization: University of Coimbra
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  surname: Boardman
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  organization: UiT the Arctic University of Norway
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  givenname: Rob C. I.
  orcidid: 0000-0003-3781-5177
  surname: Wüst
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  givenname: Terje S.
  orcidid: 0000-0003-3314-4652
  surname: Larsen
  fullname: Larsen, Terje S.
  email: terje.larsen@uit.no
  organization: UiT the Arctic University of Norway
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31840389$$D View this record in MEDLINE/PubMed
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Keywords diabetes
mitochondria
heart
lipotoxicity
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e_1_2_9_13_1
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Cook S (e_1_2_9_205_1) 2003; 133
e_1_2_9_230_1
e_1_2_9_253_1
e_1_2_9_291_1
e_1_2_9_127_1
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e_1_2_9_86_1
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Snippet Obesity‐induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this...
Obesity-induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this...
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SubjectTerms Bioenergetics
Cardiomyopathy
Diabetes
Diabetes mellitus (non-insulin dependent)
heart
Insulin
Insulin resistance
lipotoxicity
Medical disciplines: 700
Medisinske Fag: 700
Metabolism
Mitochondria
Non-pharmacological intervention
Oxidation
Oxidative phosphorylation
Phosphorylation
VDP
Title Altered mitochondrial metabolism in the insulin‐resistant heart
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fapha.13430
https://www.ncbi.nlm.nih.gov/pubmed/31840389
https://www.proquest.com/docview/2358163149
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