Altintas Fatih, Caliskan Sadettin, Tunc-Ata Melek, Kilic-Toprak Emine, Tokgun Onur, Avci Neslihan Esra, Kucukatay Vural
Department of Physiology, Faculty of Medicine, Pamukkale University, Denizli, Turkey.
Department of Physiology, Faculty of Medicine, Üsküdar University, İstanbul, Turkey.
Iran J Basic Med Sci. 2023;26(11):1265-1271. doi: 10.22038/IJBMS.2023.70711.15369.
The detrimental effects of high fructose consumption on metabolic health have been extensively studied. However, limited research has focused on the impact of fructose intake on neuroprotective mechanisms, specifically the expression of insulin receptor (INSR) and glucagon-like peptide-1 receptor (GLP-1R) in the hippocampus. Understanding the effects of fructose on these neuroprotective molecules can provide valuable insights into the potential role of fructose in hippocampal dysfunction. The goal of this study is to aim at the basal plasma levels of lipid profile, insulin, GLP-1, and HOMA-IR, as well as the mRNA and protein expression of neuroprotective molecules such as INSR and GLP-1R in Wistar rats fed a high fructose diet.
Rats were separated into control (C) and high fructose (HF) groups. The HF group was given 20% fructose water to drink for 16 weeks.
Fructose ingestion significantly increased abdominal fat (C=1.24±0.08 g, HF=1.79±0.19 g, 0.05) and plasma triglyceride levels (C=179.22±22.85 µg/ml, HF=242.45±14.45 µg/ml, 0.05), but had no statistically significant effect on body weight and plasma HDL, LDL, total cholesterol, insulin, and GLP-1 levels (0.05). Although INSR mRNA expression in the hippocampus was significantly lower in the HF group compared to the control group (0.05), GLP-1R mRNA expression did not differ significantly across the groups (0.05). Furthermore, whereas INSR and GLP-1R protein levels in the experimental group were on a declining trend, this trend was not substantially different (0.05).
These data suggest that fructose consumption may be harmful to the hippocampus by lowering the expression of INSR.
高果糖摄入对代谢健康的有害影响已得到广泛研究。然而，关于果糖摄入对神经保护机制的影响，特别是对海马体中胰岛素受体（INSR）和胰高血糖素样肽-1受体（GLP-1R）表达的影响，研究相对较少。了解果糖对这些神经保护分子的作用，可为果糖在海马体功能障碍中的潜在作用提供有价值的见解。本研究旨在观察喂食高果糖饮食的Wistar大鼠的基础血脂、胰岛素、GLP-1水平以及HOMA-IR，以及神经保护分子如INSR和GLP-1R的mRNA和蛋白表达情况。
将大鼠分为对照组（C）和高果糖组（HF）。高果糖组给予20%果糖水溶液饮用16周。
摄入果糖显著增加了腹部脂肪（C组=1.24±0.08克，HF组=1.79±0.19克，P<0.05）和血浆甘油三酯水平（C组=179.22±22.85微克/毫升，HF组=242.45±14.45微克/毫升，P<0.05），但对体重以及血浆高密度脂蛋白、低密度脂蛋白、总胆固醇、胰岛素和GLP-1水平无统计学显著影响（P>0.05）。尽管与对照组相比，高果糖组海马体中INSR的mRNA表达显著降低（P<0.05），但各组间GLP-1R的mRNA表达无显著差异（P>0.05）。此外，虽然实验组中INSR和GLP-1R的蛋白水平呈下降趋势，但这种趋势差异不显著（P>0.05）。
这些数据表明，摄入果糖可能通过降低INSR的表达对海马体产生有害影响。
