Translational machinery of mitochondrial mRNA is promoted by physical activity in Western diet-induced obese mice
Aim Mitochondria‐encoded proteins are necessary for oxidative phosphorylation; however, no report has examined how physical activity (PA) and obesity affect mitochondrial mRNA translation machinery. Our purpose was to determine whether Western diet (WD)‐induced obesity and voluntary wheel running (V...
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Veröffentlicht in: | Acta Physiologica 2016-11, Vol.218 (3), p.167-177 |
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Zusammenfassung: | Aim
Mitochondria‐encoded proteins are necessary for oxidative phosphorylation; however, no report has examined how physical activity (PA) and obesity affect mitochondrial mRNA translation machinery. Our purpose was to determine whether Western diet (WD)‐induced obesity and voluntary wheel running (VWR) impact mitochondrial mRNA translation machinery and whether expression of this machinery is dictated by oxidative phenotype.
Methods
Obesity was induced with 8‐wk WD feeding, and in the final 4 wks, half of mice were allowed VWR. Mitochondrial mRNA translation machinery including initiation factors (mtIF2/3), elongation factor Tu (TUFM) and translational activator (TACO1), and mitochondria‐encoded proteins (CytB and ND4) was assessed by immunoblotting. The relation of mitochondrial mRNA translation to muscle oxidative phenotype was assessed using PGC‐1α transgenic overexpression (MCK‐PGC‐1α vs. wild‐type mice) and comparing across muscle groups in wild‐type mice.
Results
mtIF3 and TACO1 proteins were ~45% greater in VWR than sedentary (SED), and TACO1 and mtIF2 proteins were ~60% and 125% greater in WD than normal chow (NC). TUFM protein was ~50% lower in WD‐SED than NC‐SED, but ~50% greater in WD‐VWR compared to NC‐SED. CytB and ND4 were ~40% greater in VWR and ND4 was twofold greater with WD. TUFM, TACO1, ND4 and CytB were greater in MCK‐PGC‐1α compared to wild‐type, and mtIF2/3 contents were not different. In oxidative muscle (soleus), mitochondrial translation machinery was elevated compared to mixed (gastrocnemius) or glycolytic (extensor digitorum longus) muscles.
Conclusion
These data suggest a novel mechanism promoting mitochondrial function by translation of mitochondrial protein following PA. This may act to promote muscle health by PA in obesity. |
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ISSN: | 1748-1708 1748-1716 |
DOI: | 10.1111/apha.12687 |