NDLI: Sarcolipin expression is not required for the mitochondrial enzymatic response to physical activity or diet.

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Year: 2017 Volume: 122

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Sarcolipin expression is not required for the mitochondrial enzymatic response to physical activity or diet.

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Sarcolipin expression is not required for the mitochondrial enzymatic response to physical activity or diet.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gamu, Daniel Trinh, Anton Farjado, Val A. Bombardier, Eric Tupling, A. Russell
Description	Author Affiliation: Gamu D ( University of Waterloo.); Trinh A ( University of Waterloo.); Farjado VA ( Brock University.); Bombardier E ( University of Waterloo.); Tupling AR ( Waterloo University, Canada rtupling@uwaterloo.ca.)
Abstract	In mice, transgenic manipulation of Ca -handling proteins is sufficient to alter the metabolic phenotype of muscle. We have previously shown that ablation of sarcolipin (SLN), a regulatory protein and uncoupler of sarco(endo)plasmic reticulum Ca -ATPases, leads to excessive diet-induced obesity and glucose intolerance in mice. However, it is unclear how loss of SLN per se affects muscle oxidative capacity and the ability of mitochondria to adapt to physiological stimuli such as exercise training or calorie overload. To address this, Sln and wild-type (WT) littermates were given access to voluntary running wheels or underwent a treadmill training protocol for 8 weeks. Furthermore, a separate group of mice were given a high-fat diet (42%kcal from fat for 8 weeks) to determine if the excessively obese phenotype of Sln mice is associated with altered oxidative capacity. While voluntary running was insufficient to elicit mitochondrial adaptations, treadmill trained mice showed significant increases (P <0.05) in the maximal activities of succinate dehydrogenase (+11%), citrate synthase (+12%), cytochrome oxidase (COX: +17%), along with increased protein expression of cytochrome-c (+34%) and COXIV (+28%), which were irrespective of SLN expression. Lastly, no changes in the activities of mitochondrial marker enzymes existed with high-fat feeding, regardless of genotype. Together, these findings indicate that SLN is not overtly involved in the regulation of oxidative capacity in response to physiological stress, namely exercise or caloric surfeit.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
Journal	Journal of Applied Physiology
Language	English
Publisher	American Physiological Society
Publisher Date	2017-02-09
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Applied Physiology Molecular Biology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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