Cinnamon intake alleviates the combined effects of dietary-induced insulin resistance and acute stress on brain mitochondria

Abstract

Insulin resistance (IR), which is a leading cause of the metabolic syndrome, results in early brain function alterations which may alter brain mitochondrial functioning. Previously, we demonstrated that rats fed a control diet and submitted to an acute restraint stress exhibited a delayed mitochondrial permeability transition pore (mPTP) opening. In this study, we evaluated the combined effects of dietary and emotional stressors as found in western way of life. We studied, in rats submitted or not to an acute stress, the effects of diet-induced IR on brain mitochondria, using a high fat/high fructose diet (HF2), as an IR inducer, with addition or not of cinnamon as an insulin sensitizer. We measured Ca2+ retention capacity, respiration, ROS production, enzymatic activities and cell signaling activation. Under stress, HF2 diet dramatically decreased the amount of Ca2+ required to open the mPTP (13%) suggesting an adverse effect on mitochondrial survival. Cinnamon added to the diet corrected this negative effect and resulted in a partial recovery (30%). The effects related to cinnamon addition to the diet could be due to its antioxidant properties or to the observed modulation of PI3K-AKT-GSK3β and MAPK-P38 pathways or to a combination of both. These data suggest a protective effect of cinnamon on brain mitochondria against the negative impact of an HF2 diet. Cinnamon could be beneficial to counteract deleterious dietary effects in stressed conditions.