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

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• 作者：Karine Couturier^a ; ^b ; Isabelle Hininger^a ; ^b ; Laurent Poulet^a ; ^b ; Richard A. Anderson^c ; ¹ ; Anne-Marie Roussel^a ; ^b ; Fré ; dé ; ric Canini^d ; ^e ; Cé ; cile Batandier^a ; ^b ; ^{Cecile.Batandier@ujf-grenoble.fr" class="auth_mail" title="E-mail the corresponding author}
• 关键词：mPTP ; mitochondrial Permeability Transition Pore ; CRC ; Calcium Retention Capacity ; C ; Control ; C/S ; Control with Stress ; C+Cn ; Control plus Cinnamon ; C+Cn/S ; Control plus Cinnamon with Stress ; HF2 ; High Fat/High Fructose ; HF2/S ; High Fat/High Fructose with Stress ; HF2+Cn ; High Fat/High Fructose plus Cinnamon ; HF2+Cn/S ; High Fat/High Fructose plus Cinnamon with Stress ; ETC ; Electron Transport Chain ; IR ; Insulin-Resistant or Insulin-Resistance ; P/T ; Phosphorylated/Total protein ratio ; AMPK ; Adenos
• 刊名：Journal of Nutritional Biochemistry
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：28
• 期：Complete
• 页码：183-190
• 全文大小：3111 K

文摘

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.