Physical activity prevents alterations in mitochondrial ultrastructure and glucometabolic parameters in a high-sugar diet model.
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2017
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Abstract
Endurance exercise is a remarkable intervention for the treatment of many diseases. Mitochondrial
changes on skeletal muscle are likely important for many of the benefits provided
by exercise. In this study, we aimed to evaluate the effects that a regular physical activity
(swimming without workload) has on mitochondrial morphological alterations and glucometabolic
parameters induced by a high-sugar diet (HSD). Weaned male Wistar rats fed with a
standard diet or a HSD (68% carbohydrate) were subjected to 60 minutes of regular physical
activity by swimming (without workload) for four- (20 sessions) or eight-week (40 sessions)
periods. After training, animals were euthanized and the sera, adipose tissues, and skeletal
muscles were collected for further analysis. The HSD increased body weight after an 8-
week period; it also increased the fat pads and the adipose index, resulting in glucose intolerance
and insulin resistance (IR). Transmission electron microscopy showed an increase
in alterations of mitochondrial ultrastructure in the gastrocnemius muscle, as well as a
decrease in superoxide dismutase (SOD) activity, and an increase in protein carbonylation.
Regular physical activity partially reverted these alterations in rats fed a HSD, preventing
mitochondrial morphological alterations and IR. Moreover, we observed a decrease in
Pgc1α expression (qPCR analysis) in STD-EXE group and a less pronounced reduction in
HSD-EXE group after an 8-week period. Thus, regular physical activity (swimming without
workload) in rats fed a HSD can prevent mitochondrial dysfunction and IR, highlighting the
crucial role for physical activity on metabolic homeostasis.
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QUEIROZ, K. B. et al. Physical activity prevents alterations in mitochondrial ultrastructure and glucometabolic parameters in a high-sugar diet model. PLoS One, v. 12, p. e0172103, 2017. Disponível em: <http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0172103>. Acesso em: 29 ago. 2017.