MiPsummer Programme pdf - Mitochondrial Physiology Society

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58 The Implications of Apolipoprotein E Deficiency on Cardiac Mitochondrial Oxygen Consumption. C. Rocha 1 , C. Scheede-Bergdahl 2 and A. Bergdahl 1 1 Department of Exercise Science, Concordia University, Montreal, Canada, 2 Department of Kinesiology and Physical Education, McGilll University, Montreal, , Canada, Methods: 2 month old female, age-matched C57Bl/6 (Control) or ApoE-/-- (Experimental) mice were used. Mitochondrial OXPHOS capacity was measured in permeabilizep ed cardiomyocytes by high-resolution respirometry in a cross-sectional design. Mitochondrial content was assessed by citrate synthase activity and immunoblottings of the voltage-dependent anion channel. Furtherr immunoblottings weree done to determine thee relative expressions of o the 5 OXPHOS complexes. Background: Apolipoprotein E (ApoE) is a class of macromolecules foundd in chylomicrons and low- and intermediate-density lipoproteins. They are essential for normal n catabolism of triglyceride- rich substances and are, as such, determinants of lipid metabolism m. Absence or structural mutations of ApoE will result in impaired plasma clearance of cholesterol andd triglycerides. As a consequence, lipids will be shunted into non-oxidative pathways that ultimately disrupt normal cellular function. Objectives: The objective for this project was to determine the effects of disturbed ApoE mediatedd metabolismm on mitochondrial oxidative capacity. Results: The in-situ study of mitochondrial function revealed a highly significant, , 50% decrease (p=0.002) state 2 respiration (basal, ADPstate 3 restricted) in the ApoE-/- mice whereas the (maximal, ADP stimulated) respiration was similar in both groups. Furthermore the respiratory r control ratio was 15% higher (p=0.05) in i the heartt tissue from the ApoE-/- mice while the mitochondrial leak, estimated as antimycin A flux f subtracted by oligomycin flux was reduced by 11% (p=0.05). Abstract # 29 Conclusion: The results indicate that lack of ApoE, even in youngg animals, will affect the coupling between oxidation and phosphorylation within the cardiac mitochondria. Additional work is necessary to clarify the potential damaging effects of this reprogramming of bioenergetics. Modified substrate metabolism followingg a lack of ApoE and subsequent augmentation of cholesteroll and triglyceride levels, seems to initially alter the energetic demands off the heart. Additional studies need to be performed too define the functionall underpinnings and whether this condition ultimately contributes to t heart failure.
59 Thursday 29 th Models, Structure and Function Abstracts # 30 – 36
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COPENHAGEN MiP SUMMER 2013 MITOCHON
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3 MiPs - The Mitochondrial Physiolo
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5 Finding your way at the Panum Ins
Page 7 and 8: 7 PANUM INSTITUTE HOTEL ØSTERPORT
Page 9 and 10: 9 Afternoon programme Monday 26th A
Page 11 and 12: 11 Poster walk/talk The poster sess
Page 13 and 14: 13 Overview of workshops Tuesday, A
Page 15 and 16: 15 Overview of workshops Thursday,
Page 17 and 18: 17 Participants Adelheid Weidinger
Page 19 and 20: 19 Participants Giulia Girolimetti
Page 21 and 22: 21 Participants Michel van Schaarde
Page 23 and 24: 23 Speakers Albert Gjedde Universit
Page 25 and 26: 25 Organizers & teachers Bjørn Qui
Page 27 and 28: 27 Abstract # 1 Nicotinamide phosph
Page 29 and 30: 29 Abstract # 3 Aerobic interval tr
Page 31 and 32: 31 Abstract # 5 The progressive eff
Page 33 and 34: 33 Abstract # 7 Exercise with low g
Page 35 and 36: 35 Tuesday 27 th Aging, Development
Page 37 and 38: 37 Abstract # 10 Overexpression of
Page 39 and 40: 39 Abstract # 12 Physical Propertie
Page 41 and 42: 41 Abstract # 14 MITOCHONDRIAL RHOM
Page 43 and 44: 43 Tuesday 27 th Neuro Abstracts #
Page 45 and 46: 45 Abstract # 17 Mitochondrial comp
Page 47 and 48: 47 Abstract # 19 Over Expression of
Page 49 and 50: 49 Abstract # 21 Flux control analy
Page 51 and 52: 51 Abstract # 23 Developing models
Page 53 and 54: 53 Abstract # 24 Reperfusion-induce
Page 55 and 56: 55 Abstract # 26 Myocardial Fatty A
Page 57: 57 Time dependence of diet-induced
Page 61 and 62: 61 Abstract # 31 Generation of a Dr
Page 63 and 64: 63 Abstract # 33 The human N-termin
Page 65 and 66: 65 Abstract # 35 Mitochondrial memb
Page 67 and 68: 67 Thursday 29 th Inflammation, Oxi
Page 69 and 70: 69 Abstract # 38 Evidence that fibr
Page 71 and 72: 71 Abstract # 40 Linking placental
Page 73 and 74: 73 Abstract # 42 CVB3-induced oxida
Page 75 and 76: 75 Abstract # 43 Metabolic flexibil
Page 77 and 78: 77 Abstract # 45 Dietary restrictio
Page 79 and 80: 79 Abstract # 47 Insulin sensitivit
Page 81 and 82: 81 Abstract # 49 Mitochondrial toxi
Page 83 and 84: 83 Altered mitochondrial DNA conten
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