作者: Karine Couturier , Isabelle Hininger , Laurent Poulet , Richard A Anderson , Anne-Marie Roussel
DOI: 10.1016/J.JNUTBIO.2015.10.016
关键词:
摘要: Insulin resistance (IR), which is a leading cause of the metabolic syndrome, results in early brain function alterations may alter mitochondrial functioning. Previously, we demonstrated that rats fed control diet and submitted to an acute restraint stress exhibited delayed permeability transition pore (mPTP) opening. In this study, evaluated combined effects dietary emotional stressors as found western way life. We studied, or not stress, diet-induced IR on mitochondria, using high fat/high fructose (HF(2)), inducer, with addition cinnamon insulin sensitizer. measured Ca(2+) retention capacity, respiration, ROS production, enzymatic activities cell signaling activation. Under HF(2) dramatically decreased amount required open mPTP (13%) suggesting adverse effect survival. Cinnamon added corrected negative resulted partial recovery (30%). The related could be due its antioxidant properties observed modulation PI3K-AKT-GSK3β MAPK-P38 pathways combination both. These data suggest protective mitochondria against impact diet. beneficial counteract deleterious stressed conditions.