Glban Alhadi M, Vasiljević Ana, Veličković Nataša, Nikolić-Kokić Aleksandra, Blagojević Duško, Matić Gordana, Nestorov Jelena
Department of Biochemistry, Institute for Biological Research 'Siniša Stanković', University of Belgrade, 11060, Belgrade, Serbia.
Department of Physiology, Institute for Biological Research 'Siniša Stanković', University of Belgrade, 11060, Belgrade, Serbia.
J Sci Food Agric. 2015 Aug 30;95(11):2319-24. doi: 10.1002/jsfa.6953. Epub 2014 Nov 10.
Increased fructose consumption correlates with rising prevalence of various metabolic disorders, some of which were linked to oxidative stress. The relationship between fructose consumption and oxidative stress is complex and effects of a fructose-rich diet on the young population have not been fully elucidated. The aim of this study was to investigate whether high-fructose diet applied in the period from weaning to adulthood induces oxidative stress in the liver, thus contributing to induction or aggravation of metabolic disturbances in later adulthood. To that end we examined the effects of high-fructose diet on expression and activity of antioxidant enzymes, markers of lipid peroxidation and protein damage in the liver as the main fructose metabolizing tissue.
High-fructose diet increased only SOD2 (mitochondrial manganese superoxide dismutase) activity, with no effect on other antioxidant enzymes, lipid peroxidation or accumulation of damaged proteins in the liver.
The results show that fructose-induced metabolic disturbances could not be attributed to oxidative stress, at least not at young age. The absence of oxidative stress in the liver observed herein implies that young organisms are capable of maintaining redox homeostasis when challenged by fructose-derived energy overload.
果糖摄入量增加与各种代谢紊乱患病率上升相关，其中一些与氧化应激有关。果糖摄入与氧化应激之间的关系很复杂，富含果糖的饮食对年轻人群的影响尚未完全阐明。本研究的目的是调查从断奶到成年期给予高果糖饮食是否会在肝脏中诱导氧化应激，从而导致成年后期代谢紊乱的诱发或加重。为此，我们研究了高果糖饮食对肝脏中抗氧化酶的表达和活性、脂质过氧化标志物以及蛋白质损伤的影响，肝脏是主要的果糖代谢组织。
高果糖饮食仅增加了超氧化物歧化酶2（线粒体锰超氧化物歧化酶）的活性，对其他抗氧化酶、脂质过氧化或肝脏中受损蛋白质的积累没有影响。
结果表明，果糖诱导的代谢紊乱不能归因于氧化应激，至少在年轻时不能。本文观察到的肝脏中不存在氧化应激意味着年轻生物体在受到果糖衍生的能量过载挑战时能够维持氧化还原稳态。
