Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/52917
Title: Effect of insulin on IR and GLP1-R expressions in HT22 cells
Authors: Tunc-Ata, M.
Altunay, Z.M.
Alphan, A.
Kucukatay, V.
Keywords: Glucagon-like peptide-1 receptor
HT22 cell line
Insulin receptor
glucagon like peptide 1 receptor
insulin
insulin receptor
messenger RNA
nucleotide
glucagon like peptide 1
insulin receptor
messenger RNA
phosphatidylinositol 3 kinase
animal cell
Article
controlled study
follow up
HT22 cell line
insulin signaling
mouse
nonhuman
protein expression
real time polymerase chain reaction
Western blotting
animal
genetics
Animals
Glucagon-Like Peptide 1
Insulin
Mice
Phosphatidylinositol 3-Kinases
Receptor, Insulin
RNA, Messenger
Publisher: Springer
Abstract: Insulin is a significant growth factor that specifically binds to the insulin receptor (IR) in the brain and then activates the PI3K-AKT pathway. Glucagon-like peptide 1 (GLP-1) has a variety of functions including neuroprotection, support for neurogenesis, and increasing insulin signal. This study aims to investigate the effect of insulin administered to immortalized clonal mouse hippocampal cell line (HT22) at different doses and intervals on IR, insulin receptor A (IRA), insulin receptor B (IRB), and Glucagon-like peptide 1 receptor (GLP1-R) mRNA expression and protein levels. The cells were planted in 6 well plates at a density of 3 × 105/4 × 105. Cells treated with insulin at different concentrations (5, 10, and 40 nM) were collected at 0.5, 2, 8, 16, and 24 h. RT-PCR and western blot analysis were used to measure mRNA expression and protein levels. Our results showed that insulin has short and long-term effects on IR and GLP1-R expression depending on dose and time. These findings may guide future studies targeting IR isoforms and GLP1-R in particular, as well as determining the optimal dose and duration of insulin stimulation in insulin signaling research. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
URI: https://doi.org/10.1007/s12032-023-02172-w
https://hdl.handle.net/11499/52917
ISSN: 1357-0560
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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