Cholecalciferol in ethanol-preferring rats muscle fibers increases the number and area of type II fibers
•The UChB ethanol-preferring rats used did not show myopathy or neuropathy in this experiment.•Cholecalciferol supplementation contributed to the enhancement of the glycolytic patterns of the EDL muscle.•It was found an increase in the number and area of type II fibers and a decrease in the area of...
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Veröffentlicht in: | Acta histochemica 2018-11, Vol.120 (8), p.789-796 |
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Zusammenfassung: | •The UChB ethanol-preferring rats used did not show myopathy or neuropathy in this experiment.•Cholecalciferol supplementation contributed to the enhancement of the glycolytic patterns of the EDL muscle.•It was found an increase in the number and area of type II fibers and a decrease in the area of type I fibers in de EDL muscle.
The chronic use of ethanol causes neuropathy and atrophy of type II fibers and promotes vitamin D decrease. This study evaluated cholecalciferol effects on the deep fibular nerve and extensor digitorum longus (EDL) muscle using an UChB ethanol-preferring rats model. Blood analyses were carried out to measure levels of 25-hydroxycholecalciferol (25(OH)D), calcium (Ca2+), Phosphorus (P), and parathyroid hormone (PTH). It was used EDL muscle to evaluate oxidative stress. The deep fibular nerve and EDL muscle were used for morphologic and morphometric assessment. 25(OH)D plasma levels were higher in the supplemented group and no alterations were observed in other parameters including the oxidative stress evaluation. The G ratio remained constant which indicates nervous conduction normality. Cholecalciferol supplementation promoted an increase in the number and area of type II fibers and a decrease in the area of type I fibers. In the studied model, there was neither alcoholic myopathy nor neuropathy. The EDL muscle glycolytic patterns in the high-drinker UChB rats may be associated with the differential effects of cholecalciferol on metabolism and protein synthesis in skeletal muscle. |
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ISSN: | 0065-1281 1618-0372 |
DOI: | 10.1016/j.acthis.2018.09.004 |