Altered mitochondrial metabolism in the insulin resistant heart

Marina Makrecka-Kuka, Edgars Liepinsh, Andrew J Murray, Hélène Lemieux, Maija Dambrova, Kersti Tepp, Marju Puurand, Tuuli Käämbre, Woo Hyun Han, Paul de Goede, Katie A O'Brien, Belma Turan, Erkan Tuncay, Yusuf Olgar, Anabela P Rolo, Carlos M Palmeira, Neoma T Boardman, Rob Ci Wüst, Terje S Larsen

Research output: Contribution to JournalReview articleAcademicpeer-review


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.

Original languageEnglish
Article numbere13430
Pages (from-to)e13430
JournalActa Physiologica
Issue number3
Early online date16 Dec 2019
Publication statusPublished - Mar 2020

Bibliographical note

© 2019 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.


This publication is based upon work from COST Action CA15203 MITOEAGLE, supported by COST (European Cooperation in Science and Technology). Web site: . EL was supported by Latvian Council of Science grant project no. lzp‐2018/1‐0082. KT, MP, TK were supported by the institutional research funding IUT23‐1 of the Estonian Ministry of Education and Research.

FundersFunder number
European Cooperation in Science and TechnologyCA15203
Haridus- ja Teadusministeerium
Latvijas Zinātnes Padomelzp‐2018/1‐0082


    • diabetes
    • heart
    • lipotoxicity
    • mitochondria


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