Investigation of fructose consumption on hippocampal insulin and glucagon-like peptide-1 receptors, and metabolic effects in rats
| Autor: | Fatih Altintas, Sadettin Caliskan, Melek Tunc-Ata, Emine Kilic-Toprak, Onur Tokgun, Neslihan Avci, Vural Kucukatay |
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| Jazyk: | angličtina |
| Rok vydání: | 2023 |
| Předmět: | |
| Zdroj: | Iranian Journal of Basic Medical Sciences, Vol 26, Iss 11, Pp 1265-1271 (2023) |
| Druh dokumentu: | article |
| ISSN: | 2008-3866 2008-3874 |
| DOI: | 10.22038/ijbms.2023.70711.15369 |
| Popis: | Objective(s): 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. Materials and Methods: Rats were separated into control (C) and high fructose (HF) groups. The HF group was given 20% fructose water to drink for 16 weeks. Results: Fructose ingestion significantly increased abdominal fat (C=1.24±0.08 g, HF=1.79±0.19 g, P0.05). Although INSR mRNA expression in the hippocampus was significantly lower in the HF group compared to the control group (P0.05). Furthermore, whereas INSR and GLP-1R protein levels in the experimental group were on a declining trend, this trend was not substantially different (P>0.05).Conclusion: These data suggest that fructose consumption may be harmful to the hippocampus by lowering the expression of INSR. |
| Databáze: | Directory of Open Access Journals |
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