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Cardiac mitochondrial respiration following a low-carbohydrate, high-fat diet in apolipoprotein E-deficient mice.

Authors: Rocha CKoury OHScheede-Bergdahl CBergdahl A


Affiliations

1 Department of Health, Kinesiology & Applied Physiology, Concordia University, 7141 Sherbrooke West, Montreal, QC, H4B 1R6, Canada.
2 Department of Kinesiology and Physical Education, McGill Research Centre for Physical Activity & Health, McGill University, 475 Pine Avenue West, Montreal, H2W 1S4, QC, Canada.
3 Department of Health, Kinesiology & Applied Physiology, Concordia University, 7141 Sherbrooke West, Montreal, QC, H4B 1R6, Canada. andreas.bergdahl@concordia.ca.

Description

Cardiac mitochondrial respiration following a low-carbohydrate, high-fat diet in apolipoprotein E-deficient mice.

J Physiol Biochem. 2019 Feb;75(1):65-72

Authors: Rocha C, Koury OH, Scheede-Bergdahl C, Bergdahl A

Abstract

Low-carbohydrate diets are considered to be an effective approach to weight loss and have, subsequently, grown in popularity. Despite the apparent health benefits that these diets may provide for insulin resistance, hypertension, and dyslipidemia, their implications on cardiomyocyte oxidative capacity have yet to be investigated. To evaluate the adaptations induced by a 6-week low-carbohydrate, high-fat (LCHF) diet on mitochondrial respiration, two groups of male mice were investigated: Apolipoprotein E-deficient mice on a LCHF diet (L-DIET) and apolipoprotein E-deficient mice on a regular rodent diet (CON). Heart tissue was extracted and used for high-resolution respirometry (HRR), while immunoblotting was performed to quantify mitochondrial density and complexes. The results demonstrate increased expression of all five mitochondrial subunits in the L-DIET group compared to control condition. Furthermore, HRR revealed increased efficiency of substrate consumption, implying augmented oxidative capacity in the L-DIET group. These findings further support the notion that cardiomyocytes prefer lipids as a primary fuel source, by demonstrating that the shift in metabolism caused by a LCHF diet facilitates such an environment. This provides important information regarding the effects of a LCHF on cardiomyocytes, especially when considering free radical production and heart dysfunction.

PMID: 30362048 [PubMed - indexed for MEDLINE]


Links

PubMed: https://www.ncbi.nlm.nih.gov/pubmed/30362048?dopt=Abstract