Zaki S M, Fattah S A, Hassan D S
Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Cairo, Egypt.
Fakeeh College for Medical Sciences, Jeddah, Saudi Arabia.
Folia Morphol (Warsz). 2019;78(1):124-136. doi: 10.5603/FM.a2018.0063. Epub 2018 Jul 16.
The Western-style diet is characterised by the high intake of energy- -dense foods. Consumption of either high-fructose diet or saturated fat resulted in the development of metabolic syndrome. Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Many researchers studied the effect of high-fat diet (HFD), high-fructose diet (HFruD) and high-fructose high-fat diet (HFHF) on the liver. The missing data are the comparison effect of these groups i.e. are effects of the HFHF diet on the liver more pronounced? So, this study was designed to compare the metabolic and histopathological effect of the HFD, HFruD, and HFHF on the liver. The proposed underlying mechanisms involved in these changes were also studied.
Twenty four rats were divided into four groups: con- trol, HFD, HFruD, and HFHF. Food was offered for 6 weeks. Biochemical, light microscopic, immunohistochemical (Inducible nitric oxide synthase [iNOS] and alpha-smooth muscle actin [α-SMA]), real-time polymerase chain reaction (gene expression of TNF-α, interleukin-6, Bax, BCL-2, and caspase 3), histomorphometric analysis and oxidative/antioxidative markers (thiobarbituric acid reactive substances [TBARS], malondialdehyde [MDA]/glutathione [GSH] and superoxide dismutase [SOD]) were done.
The HFD, HFruD and HFHF groups developed a cluster of liver disorders; steatosis, necrosis, inflammation, apoptosis, ballooning degeneration and cytopla- smic vacuolations. Internal metabolic impairments include elevated serum levels of glucose, triglycerides, low density lipoprotein and decreased serum levels of high density lipoprotein and albumin. The immunoreaction of the α-SMA and iNOS was strong in these groups. The oxidant markers (MDA and TBARS) were elevated, while the antioxidant markers (SOD and GSH) were decreased. The area per cent of collagen, inflammatory markers, caspase 3 and Bax were elevated, while the BCL-2/Bax ratio was decreased. The decrease in PAS, antioxidant markers and the elevation of the α-SMA, iNOS, inflammatory and oxidant markers were obvious in the HFHF when compared to that of the other groups.
High-fat diet, HFruD, and HFHF developed morphologic hepatic changes ranging from steatosis to necrosis and inflammation, besides the deve- lopment of internal metabolic impairments. The chief factors of hepatic injury were fat accumulation in the hepatocytes, oxidative stress and highly elevated iNOS. Compared to the other groups, HFHF's effect was more prominent.
西式饮食的特点是高能量密度食物的摄入量高。食用高果糖饮食或饱和脂肪都会导致代谢综合征的发生。非酒精性脂肪性肝病（NAFLD）是代谢综合征的肝脏表现。许多研究人员研究了高脂饮食（HFD）、高果糖饮食（HFruD）和高果糖高脂饮食（HFHF）对肝脏的影响。缺失的数据是这些组之间的比较效果，即HFHF饮食对肝脏的影响是否更显著？因此，本研究旨在比较HFD、HFruD和HFHF对肝脏的代谢和组织病理学影响。还研究了这些变化中涉及的潜在机制。
将24只大鼠分为四组：对照组、HFD组、HFruD组和HFHF组。给予食物6周。进行生化、光学显微镜、免疫组织化学（诱导型一氧化氮合酶[iNOS]和α-平滑肌肌动蛋白[α-SMA]）、实时聚合酶链反应（肿瘤坏死因子-α、白细胞介素-6、Bax、BCL-2和半胱天冬酶3的基因表达）、组织形态计量分析和氧化/抗氧化标志物（硫代巴比妥酸反应性物质[TBARS]、丙二醛[MDA]/谷胱甘肽[GSH]和超氧化物歧化酶[SOD]）检测。
HFD组、HFruD组和HFHF组出现了一系列肝脏疾病；脂肪变性、坏死、炎症、凋亡、气球样变性和细胞质空泡化。内部代谢障碍包括血清葡萄糖、甘油三酯、低密度脂蛋白水平升高，血清高密度脂蛋白和白蛋白水平降低。这些组中α-SMA和iNOS的免疫反应较强。氧化标志物（MDA和TBARS）升高，而抗氧化标志物（SOD和GSH）降低。胶原蛋白面积百分比、炎症标志物、半胱天冬酶3和Bax升高，而BCL-2/Bax比值降低。与其他组相比，HFHF组中PAS、抗氧化标志物的降低以及α-SMA、iNOS、炎症和氧化标志物的升高更为明显。
高脂饮食、HFruD和HFHF除了导致内部代谢障碍外，还导致了从脂肪变性到坏死和炎症的肝脏形态学变化。肝损伤的主要因素是肝细胞内脂肪堆积、氧化应激和iNOS高度升高。与其他组相比，HFHF的影响更为突出。
