Dirks, Marlou L. published the artcileShort-term bed rest-induced insulin resistance cannot be explained by increased mitochondrial H2O2 emission, SDS of cas: 97-67-6, the main research area is insulin resistance mitochondrial emission oxidative stress; bed rest; insulin resistance; mitochondria; muscle disuse; reactive oxygen species.
Key points : We determined if bed rest increased mitochondrially derived reactive oxygen species and cellular redox stress, contributing to the induction of insulin resistance. Bed rest decreased maximal and submaximal ADP-stimulated mitochondrial respiration. We investigated the potential that an increase in skeletal muscle mitochondrial H2O2 emission, potentially as a result of decreased ADP sensitivity, contributes to cellular redox stress and the induction of insulin resistance during short-term bed rest in 20 healthy males. Bed rest led to a decline in glucose infusion rate during a hyperinsulinemic-euglycemic clamp (-42 ± 2%; P < 0.001), and in permeabilized skeletal muscle fibers it decreased OXPHOS protein content (-16 ± 8%) and mitochondrial respiration across a range of ADP concentrations (-13 ± 5%). While bed rest tended to increase maximal mitochondrial H2O2 emission rates (P = 0.053), H2O2 emission in the presence of ADP concentrations indicative of resting muscle, the ratio of H2O2 emission to mitochondrial O2 consumption, and markers of oxidative stress were not altered following bed rest. Altogether, while bed rest impairs mitochondrial ADP-stimulated respiration, an increase in mitochondrial H2O2 emission does not contribute to the induction of insulin resistance following short-term bed rest. Journal of Physiology (Oxford, United Kingdom) published new progress about Carbohydrates Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, SDS of cas: 97-67-6.
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