González-Montoya Marcela, Vargas-Vargas Manuel Alejandro, Torres-Isidro Olin, García-Berumen Claudia Isabel, Cuiniche-Méndez María Guadalupe, Saavedra-Molina Alfredo, Ontiveros-Rodríguez Julio Cesar, García-Gutiérrez Hugo A, Calderón-Cortés Elizabeth, Cortés-Rojo Christian
Instituto de Investigaciones Químico-Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58030, MC, Mexico.
Consejo Nacional de Humanidades, Ciencias y Tecnologías-Instituto de Investigaciones Químico Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58030, MC, Mexico.
Metabolites. 2024 Aug 4;14(8):431. doi: 10.3390/metabo14080431.
High-fat and high-carbohydrate (HF-HC) diets induce metabolic syndrome via mitochondrial dysfunction and oxidative stress. We have previously shown that this may be prevented by avocado oil, a source of bioactive molecules with antioxidant properties. However, it is unknown if these effects are mediated by the unsaponifiable fraction of avocado oil (UFAO). Thus, we tested if this fraction improves glucose metabolism, bioenergetics and oxidative stress in mitochondria from the kidney and liver of rats fed an HF-HC diet. We found that 12 weeks of an HF-HC diet impaired glucose utilization and increased insulin resistance, which was prevented by UFAO administration. The HF-HC diet decreased respiration, membrane potential and electron transport chain (ETC) function in liver and kidney mitochondria. These mitochondrial dysfunctions were prevented by UFAO intake. Unexpectedly, UFAO increased ROS levels in the mitochondria of control animals and did not decrease them in rats with an HF-HC diet; however, UFAO protects liver and kidney mitochondria from iron-induced oxidative stress. These findings suggest that impairments in glucose metabolism and mitochondrial function by an HF-HC diet may be prevented by UFAO, without decreasing ROS generation but protecting mitochondria from oxidative damage.
高脂高碳水化合物(HF-HC)饮食通过线粒体功能障碍和氧化应激诱导代谢综合征。我们之前已经表明,鳄梨油(一种具有抗氧化特性的生物活性分子来源)可能会预防这种情况。然而,尚不清楚这些作用是否由鳄梨油的不皂化物部分(UFAO)介导。因此,我们测试了该部分是否能改善喂食HF-HC饮食的大鼠肾脏和肝脏线粒体中的葡萄糖代谢、生物能量学和氧化应激。我们发现,12周的HF-HC饮食会损害葡萄糖利用并增加胰岛素抵抗,而UFAO给药可预防这种情况。HF-HC饮食降低了肝脏和肾脏线粒体的呼吸、膜电位和电子传递链(ETC)功能。UFAO摄入可预防这些线粒体功能障碍。出乎意料的是,UFAO增加了对照动物线粒体中的ROS水平,并且在喂食HF-HC饮食的大鼠中并未降低ROS水平;然而,UFAO可保护肝脏和肾脏线粒体免受铁诱导的氧化应激。这些发现表明,UFAO可以预防HF-HC饮食引起的葡萄糖代谢和线粒体功能损害,而不会减少ROS的产生,但能保护线粒体免受氧化损伤。