Characterising the Myocardial Mitochondria Phenotype in a Murine Model of Diabetic Cardiomyopathy

Alex Malik Parker; Mitchel Tate; Darnel Prakoso; Minh Deo; Andrew M. Willis; David M. Nash; Daniel G. Donner; Simon A. Crawford; Helen Kiriazis; Cesare Granata; Melinda T. Coughlan; Miles De Blasio; Rebecca H. Ritchie

doi:10.1016/j.hlc.2021.06.058

Characterising the Myocardial Mitochondria Phenotype in a Murine Model of Diabetic Cardiomyopathy

Alex Malik Parker, Mitchel Tate, Darnel Prakoso, Minh Deo, Andrew M. Willis, David M. Nash, Daniel G. Donner, Simon A. Crawford, Helen Kiriazis, Cesare Granata, Melinda T. Coughlan, Miles De Blasio, Rebecca H. Ritchie

Research output: Contribution to journal › Meeting Abstract

Abstract

Background
Diabetes patients are at a higher risk of developing heart failure compared to patients without diabetes. In addition, mitochondrial dysfunction is a common feature of the diabetic heart. We sought to characterise the mitochondrial phenotype in a non-genetic murine model of type 2 diabetic cardiomyopathy.

Methods
FVB/N mice (6-weeks-old) received low-dose streptozotocin (3-consecutive-daily i.p. injections; 55mg/kg) followed by 26 weeks of high-fat diet (42% lipids).

Results
Diabetic mice displayed impaired glucose tolerance, elevated glycated haemoglobin (HbA1c), body weight, myocardial fibrosis, superoxide generation and reduced diastolic function. Interestingly, diabetic mice exhibited smaller mitochondria size, increased mitochondria complex-III and complex-V protein, and lower complex-II oxygen consumption.

Conclusions
Our findings suggest that this model replicates several mitochondrial changes seen in human diabetes and may assist in identifying treatments that target the mitochondria in diabetic cardiomyopathy.

Original language	English
Article number	055
Pages (from-to)	S118-S118
Number of pages	1
Journal	Heart Lung and Circulation
Volume	30
Issue number	S3
DOIs	https://doi.org/10.1016/j.hlc.2021.06.058
Publication status	Published - 1 Jan 2021

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.hlc.2021.06.058

Cite this

Parker, A. M., Tate, M., Prakoso, D., Deo, M., Willis, A. M., Nash, D. M., Donner, D. G., Crawford, S. A., Kiriazis, H., Granata, C., Coughlan, M. T., De Blasio, M., & Ritchie, R. H. (2021). Characterising the Myocardial Mitochondria Phenotype in a Murine Model of Diabetic Cardiomyopathy. Heart Lung and Circulation, 30(S3), S118-S118. Article 055. https://doi.org/10.1016/j.hlc.2021.06.058

@article{89473757ebd547888cdbba1436dc33a8,

title = "Characterising the Myocardial Mitochondria Phenotype in a Murine Model of Diabetic Cardiomyopathy",

abstract = "BackgroundDiabetes patients are at a higher risk of developing heart failure compared to patients without diabetes. In addition, mitochondrial dysfunction is a common feature of the diabetic heart. We sought to characterise the mitochondrial phenotype in a non-genetic murine model of type 2 diabetic cardiomyopathy.MethodsFVB/N mice (6-weeks-old) received low-dose streptozotocin (3-consecutive-daily i.p. injections; 55mg/kg) followed by 26 weeks of high-fat diet (42% lipids).ResultsDiabetic mice displayed impaired glucose tolerance, elevated glycated haemoglobin (HbA1c), body weight, myocardial fibrosis, superoxide generation and reduced diastolic function. Interestingly, diabetic mice exhibited smaller mitochondria size, increased mitochondria complex-III and complex-V protein, and lower complex-II oxygen consumption.ConclusionsOur findings suggest that this model replicates several mitochondrial changes seen in human diabetes and may assist in identifying treatments that target the mitochondria in diabetic cardiomyopathy.",

author = "Parker, {Alex Malik} and Mitchel Tate and Darnel Prakoso and Minh Deo and Willis, {Andrew M.} and Nash, {David M.} and Donner, {Daniel G.} and Crawford, {Simon A.} and Helen Kiriazis and Cesare Granata and Coughlan, {Melinda T.} and {De Blasio}, Miles and Ritchie, {Rebecca H.}",

year = "2021",

month = jan,

day = "1",

doi = "10.1016/j.hlc.2021.06.058",

language = "English",

volume = "30",

pages = "S118--S118",

journal = "Heart Lung and Circulation",

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number = "S3",

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TY - JOUR

T1 - Characterising the Myocardial Mitochondria Phenotype in a Murine Model of Diabetic Cardiomyopathy

AU - Parker, Alex Malik

AU - Tate, Mitchel

AU - Prakoso, Darnel

AU - Deo, Minh

AU - Willis, Andrew M.

AU - Nash, David M.

AU - Donner, Daniel G.

AU - Crawford, Simon A.

AU - Kiriazis, Helen

AU - Granata, Cesare

AU - Coughlan, Melinda T.

AU - De Blasio, Miles

AU - Ritchie, Rebecca H.

PY - 2021/1/1

Y1 - 2021/1/1

N2 - BackgroundDiabetes patients are at a higher risk of developing heart failure compared to patients without diabetes. In addition, mitochondrial dysfunction is a common feature of the diabetic heart. We sought to characterise the mitochondrial phenotype in a non-genetic murine model of type 2 diabetic cardiomyopathy.MethodsFVB/N mice (6-weeks-old) received low-dose streptozotocin (3-consecutive-daily i.p. injections; 55mg/kg) followed by 26 weeks of high-fat diet (42% lipids).ResultsDiabetic mice displayed impaired glucose tolerance, elevated glycated haemoglobin (HbA1c), body weight, myocardial fibrosis, superoxide generation and reduced diastolic function. Interestingly, diabetic mice exhibited smaller mitochondria size, increased mitochondria complex-III and complex-V protein, and lower complex-II oxygen consumption.ConclusionsOur findings suggest that this model replicates several mitochondrial changes seen in human diabetes and may assist in identifying treatments that target the mitochondria in diabetic cardiomyopathy.

AB - BackgroundDiabetes patients are at a higher risk of developing heart failure compared to patients without diabetes. In addition, mitochondrial dysfunction is a common feature of the diabetic heart. We sought to characterise the mitochondrial phenotype in a non-genetic murine model of type 2 diabetic cardiomyopathy.MethodsFVB/N mice (6-weeks-old) received low-dose streptozotocin (3-consecutive-daily i.p. injections; 55mg/kg) followed by 26 weeks of high-fat diet (42% lipids).ResultsDiabetic mice displayed impaired glucose tolerance, elevated glycated haemoglobin (HbA1c), body weight, myocardial fibrosis, superoxide generation and reduced diastolic function. Interestingly, diabetic mice exhibited smaller mitochondria size, increased mitochondria complex-III and complex-V protein, and lower complex-II oxygen consumption.ConclusionsOur findings suggest that this model replicates several mitochondrial changes seen in human diabetes and may assist in identifying treatments that target the mitochondria in diabetic cardiomyopathy.

U2 - 10.1016/j.hlc.2021.06.058

DO - 10.1016/j.hlc.2021.06.058

M3 - Meeting Abstract

SN - 1443-9506

VL - 30

SP - S118-S118

JO - Heart Lung and Circulation

JF - Heart Lung and Circulation

IS - S3

M1 - 055

ER -