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Difference between revisions of "Lemieux 2019b MiP2019"

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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 oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from fatty acid-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 oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from fatty acid-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.
|editor=[[Plangger M]], [[Tindle-Solomon L]]
|editor=[[Plangger M]], [[Tindle-Solomon L]]
|mipnetlab=CA Edmonton Lemieux H
}}
}}
{{Labeling
{{Labeling
|organism=Other invertebrates
|area=Exercise physiology;nutrition;life style, Pharmacology;toxicology
|diseases=Diabetes
|tissues=Heart
}}
}}
== Affiliations ==
== Affiliations ==
::::Makrecka-Kuka M(1), Liepinsh E(1), Murray AJ(2), Lemieux H(3), Dambrova M(1), Tepp K(4), Puurand M(4), Käämbre T(4), Han WH(5), de Goede P(6), O’Brien KA(2), Turan B(6), Tuncay E(7), Olgar Y(7), Rolo AP(8), Palmeira CM(8), Boardman NT(9), Wüst RCI(10), Larsen TS(9)  
::::Makrecka-Kuka M(1), Liepinsh E(1), Murray AJ(2), Lemieux H(3), Dambrova M(1), Tepp K(4), Puurand M(4), Käämbre T(4), Han WH(5), de Goede P(6), O’Brien KA(2), Turan B(6), Tuncay E(7), Olgar Y(7), Rolo AP(8), Palmeira CM(8), Boardman NT(9), Wüst RCI(10), Larsen TS(9)  


::::#Latvian Institute of Organic Synthesis, Riga, Latvia  
::::#Latvian Inst Organic Synthesis, Riga, Latvia  
::::#Department of Physiology, Development and Neuroscience, University of Cambridge, UK  
::::#Dept Physiology, Development Neuroscience, Univ Cambridge, UK  
::::#Faculty Saint-Jean, Women and Children's Health Research Institute, Department of Medicine, University of Alberta, Canada  
::::#Fac Saint-Jean, Women Children's Health Research Inst, Dept Medicine, Univ Alberta, Canada  
::::#National Institute of Chemical Physics and Biophysics, Tallinn, Estonia  
::::#National Inst Chemical Physics Biophysics, Tallinn, Estonia  
::::#Faculty Saint-Jean University of Alberta, Canada  
::::#Fac Saint-Jean Univ Alberta, Canada  
::::#Laboratory of Endocrinology, Amsterdam University Medical Center, University of Amsterdam, Amsterdam Gastroenterology & Metabolism, Amsterdam, The Netherlands  
::::#Lab Endocrinology, Amsterdam Univ Medical Center, Univ Amsterdam, Amsterdam Gastroenterology & Metabolism, Amsterdam, The Netherlands  
::::#Department of Biophysics, Faculty of Medicine, Ankara University, Ankara, Turkey  
::::#Dept Biophysics, Fac Medicine, Ankara Univ, Ankara, Turkey  
::::#Department of Life Sciences, University of Coimbra and Center for Neurosciences and Cell Biology, University of Coimbra, Portugal  
::::#Dept Life Sciences, Univ Coimbra Center Neurosciences Cell Biology, Univ Coimbra, Portugal  
::::#Cardiovascular Research Group, Department of Medical Biology, UiT the Arctic University of Norway  
::::#Cardiovascular Research Group, Dept Medical Biology, UiT the Arctic Univ Norway  
::::#Laboratory for Myology, Faculty of Behavioural and Movement Sciences, Department of Human Movement Sciences, Amsterdam Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
::::#Lab Myology, Fac Behavioural Movement Sciences, Dept Human Movement Sciences, Amsterdam Movement Sciences, Vrije Univ Amsterdam, Amsterdam, The Netherlands

Latest revision as of 13:36, 26 September 2019

Hélène Lemieux
Altered mitochondrial metabolism in the diabetic heart.

Link: MiP2019

Makrecka-Kuka M, Liepinsh E, Murray AJ, Lemieux H, Dambrova M, Tepp K, Puurand M4 Kaambre T, Han WH, de Goede P, O’Brien KA, Turan B, Tuncay E, Olgar Y, Rolo AP, Palmeira CM, Boardman NT, Wuest RCI, Larsen TS (2019)

Event: MiP2019

COST Action MitoEAGLE

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 oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from fatty acid-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.


Bioblast editor: Plangger M, Tindle-Solomon L


Labels: MiParea: Exercise physiology;nutrition;life style, Pharmacology;toxicology  Pathology: Diabetes 


Tissue;cell: Heart 





Affiliations

Makrecka-Kuka M(1), Liepinsh E(1), Murray AJ(2), Lemieux H(3), Dambrova M(1), Tepp K(4), Puurand M(4), Käämbre T(4), Han WH(5), de Goede P(6), O’Brien KA(2), Turan B(6), Tuncay E(7), Olgar Y(7), Rolo AP(8), Palmeira CM(8), Boardman NT(9), Wüst RCI(10), Larsen TS(9)
  1. Latvian Inst Organic Synthesis, Riga, Latvia
  2. Dept Physiology, Development Neuroscience, Univ Cambridge, UK
  3. Fac Saint-Jean, Women Children's Health Research Inst, Dept Medicine, Univ Alberta, Canada
  4. National Inst Chemical Physics Biophysics, Tallinn, Estonia
  5. Fac Saint-Jean Univ Alberta, Canada
  6. Lab Endocrinology, Amsterdam Univ Medical Center, Univ Amsterdam, Amsterdam Gastroenterology & Metabolism, Amsterdam, The Netherlands
  7. Dept Biophysics, Fac Medicine, Ankara Univ, Ankara, Turkey
  8. Dept Life Sciences, Univ Coimbra Center Neurosciences Cell Biology, Univ Coimbra, Portugal
  9. Cardiovascular Research Group, Dept Medical Biology, UiT the Arctic Univ Norway
  10. Lab Myology, Fac Behavioural Movement Sciences, Dept Human Movement Sciences, Amsterdam Movement Sciences, Vrije Univ Amsterdam, Amsterdam, The Netherlands