Pileggi 2016 Abstract MitoFit Science Camp 2016: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=Voluntary exercise prevents high fat diet-induced cardiac mitochondrial dysfunction in male rats | |title=Voluntary exercise prevents high fat diet-induced cardiac mitochondrial dysfunction in male rats. | ||
|info=[[File:PileggiC.jpg|right|150px|Chantal Pileggi]] | |||
|authors=Pileggi C, Hedges CP, Vickers MH, McGlashan SR, Hickey AJR, Cameron-Smith D, Firth EC, Gray C | |authors=Pileggi C, Hedges CP, Vickers MH, McGlashan SR, Hickey AJR, Cameron-Smith D, Firth EC, Gray C | ||
|year=2016 | |year=2016 | ||
|event=MitoFit | |event=MitoFit Science Camp 2016 Kuehtai AT | ||
|abstract=Obesity, hyperlipidemia and hypertension are all major risk factors for the development of cardiovascular diseases. Of the multiple cardiac aetiologies, cardiac mitochondrial dysfunction is a critical factor in the progression of heart disease. Exercise provides many beneficial health effects and is recommended for the prevention and management of cardiovascular disease. Therefore, this study aimed to determine the impact of voluntary exercise on rats fed a high-fat diet on mitochondrial metabolism of carbohydrate- and lipid-based substrates in cardiac tissue. | |abstract=Obesity, hyperlipidemia and hypertension are all major risk factors for the development of cardiovascular diseases. Of the multiple cardiac aetiologies, cardiac mitochondrial dysfunction is a critical factor in the progression of heart disease. Exercise provides many beneficial health effects and is recommended for the prevention and management of cardiovascular disease. Therefore, this study aimed to determine the impact of voluntary exercise on rats fed a high-fat diet on mitochondrial metabolism of carbohydrate- and lipid-based substrates in cardiac tissue. | ||
Weanling Sprague-Dawley male rats (aged 21 days (D21)) were allocated to receive either a standard chow diet(CD) or a high fat (HF) diet (45% kcal as fat) and fed ''ad-libitum'' and then further subdivided into sedentary (cage only exercise) (CD, HFD) or voluntary exercise groups (CDEX, HFEX) from days 64-120. Mitochondrial oxygen (O<sub>2</sub>) consumption was measured in permeabilized myofibers prepared from samples of the right atrial appendage. | Weanling Sprague-Dawley male rats (aged 21 days (D21)) were allocated to receive either a standard chow diet(CD) or a high fat (HF) diet (45% kcal as fat) and fed ''ad-libitum'' and then further subdivided into sedentary (cage only exercise) (CD, HFD) or voluntary exercise groups (CDEX, HFEX) from days 64-120. Mitochondrial oxygen (O<sub>2</sub>) consumption was measured in permeabilized myofibers prepared from samples of the right atrial appendage. | ||
Cardiac tissue from the HFD sedentary rats displayed a 1.3-fold decrease in | Cardiac tissue from the HFD sedentary rats displayed a 1.3-fold decrease in Complex I (CI) and Complex II (CII) oxidation of pyruvate and succinate, an effect that was reversed with exercise in the HFEX rats (p<0.05). Moreover, hearts from HFD and HFEX rats exhibited decreased mitochondrial oxidation of palmitoyl carnitine, malate, and succinate (p<0.05). Cardiac tissue from CDEX rats maintained similar respiratory levels as CD sedentary rats. Furthermore, expression of the mitochondrial transcription factor proliferator-activated receptor γ coacitvator α (PGC1α) was downregulated in sedentary HFD rats, but normalised in HFEX rats (''p''<0.05), suggesting that voluntary exercise may protect cardiac mitochondria during HFD. | ||
These data show that HFD-induced mitochondrial dysfunction results in specific impairments in CI + CII maximal capacity to oxidize pyruvate and succinate as substrates in cardiac tissue, which is prevented by the introduction of exercise. We also provide evidence of altered mitochondrial transcription factor expression which may be one component of the adaptive responses within cardiac muscle facilitating an increased mitochondrial oxidative capacity. | These data show that HFD-induced mitochondrial dysfunction results in specific impairments in CI + CII maximal capacity to oxidize pyruvate and succinate as substrates in cardiac tissue, which is prevented by the introduction of exercise. We also provide evidence of altered mitochondrial transcription factor expression which may be one component of the adaptive responses within cardiac muscle facilitating an increased mitochondrial oxidative capacity. | ||
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|injuries=Mitochondrial disease | |injuries=Mitochondrial disease | ||
|diseases=Cardiovascular | |diseases=Cardiovascular | ||
| | |pathways=F, N, NS | ||
|additional=MitoFit | |event=D2 | ||
|additional=MitoFit Science Camp 2016 | |||
}} | }} | ||
== Affiliations == | == Affiliations == | ||
1-Liggins Inst, Univ Auckland; 2-College Sport Exercise Sc, Victoria Univ, Australia; 3-Applied Surgery Metabolism Lab, School Biol Sc, Univ of Auckland; 4-Dept Anatomy with Radiology, Univ Auckland, New Zealand; 5-Dept Paediatrics Child Health, Wellington. Univ Otago; New Zealand. - [email protected] | 1-Liggins Inst, Univ Auckland; 2-College Sport Exercise Sc, Victoria Univ, Australia; 3-Applied Surgery Metabolism Lab, School Biol Sc, Univ of Auckland; 4-Dept Anatomy with Radiology, Univ Auckland, New Zealand; 5-Dept Paediatrics Child Health, Wellington. Univ Otago; New Zealand. - [email protected] | ||
Latest revision as of 09:49, 8 November 2016
| Has title::Voluntary exercise prevents high fat diet-induced cardiac mitochondrial dysfunction in male rats. |
Link:
Was written by::Pileggi C, Was written by::Hedges CP, Was written by::Vickers MH, Was written by::McGlashan SR, Was written by::Hickey AJR, Was written by::Cameron-Smith D, Was written by::Firth EC, Was written by::Gray C (Was submitted in year::2016)
Event: Was submitted to event::MitoFit Science Camp 2016 Kuehtai AT
[[has abstract::Obesity, hyperlipidemia and hypertension are all major risk factors for the development of cardiovascular diseases. Of the multiple cardiac aetiologies, cardiac mitochondrial dysfunction is a critical factor in the progression of heart disease. Exercise provides many beneficial health effects and is recommended for the prevention and management of cardiovascular disease. Therefore, this study aimed to determine the impact of voluntary exercise on rats fed a high-fat diet on mitochondrial metabolism of carbohydrate- and lipid-based substrates in cardiac tissue.
Weanling Sprague-Dawley male rats (aged 21 days (D21)) were allocated to receive either a standard chow diet(CD) or a high fat (HF) diet (45% kcal as fat) and fed ad-libitum and then further subdivided into sedentary (cage only exercise) (CD, HFD) or voluntary exercise groups (CDEX, HFEX) from days 64-120. Mitochondrial oxygen (O2) consumption was measured in permeabilized myofibers prepared from samples of the right atrial appendage. Cardiac tissue from the HFD sedentary rats displayed a 1.3-fold decrease in Complex I (CI) and Complex II (CII) oxidation of pyruvate and succinate, an effect that was reversed with exercise in the HFEX rats (p<0.05). Moreover, hearts from HFD and HFEX rats exhibited decreased mitochondrial oxidation of palmitoyl carnitine, malate, and succinate (p<0.05). Cardiac tissue from CDEX rats maintained similar respiratory levels as CD sedentary rats. Furthermore, expression of the mitochondrial transcription factor proliferator-activated receptor γ coacitvator α (PGC1α) was downregulated in sedentary HFD rats, but normalised in HFEX rats (p<0.05), suggesting that voluntary exercise may protect cardiac mitochondria during HFD.
These data show that HFD-induced mitochondrial dysfunction results in specific impairments in CI + CII maximal capacity to oxidize pyruvate and succinate as substrates in cardiac tissue, which is prevented by the introduction of exercise. We also provide evidence of altered mitochondrial transcription factor expression which may be one component of the adaptive responses within cardiac muscle facilitating an increased mitochondrial oxidative capacity.]]
• O2k-Network Lab: Was published by MiPNetLab::NZ Auckland Hickey AJ
Labels: MiParea: MiP area::Respiration, MiP area::Exercise physiology;nutrition;life style Pathology: Diseases::Cardiovascular Stress:Injury and adaptation::Mitochondrial disease Organism: Organism::Rat Tissue;cell: tissue and cell::Heart Preparation: Preparation::Permeabilized tissue
Pathway: Pathways::F, Pathways::N, Pathways::NS
Event: Event::D2 additional label::MitoFit Science Camp 2016
Affiliations
1-Liggins Inst, Univ Auckland; 2-College Sport Exercise Sc, Victoria Univ, Australia; 3-Applied Surgery Metabolism Lab, School Biol Sc, Univ of Auckland; 4-Dept Anatomy with Radiology, Univ Auckland, New Zealand; 5-Dept Paediatrics Child Health, Wellington. Univ Otago; New Zealand. - [email protected]
