Fibroblast growth factor-21: Preserving cell viability in diabetic neuropathy through the AKT/PI3K cellular pathway

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dc.contributor.authorTekin, Suat
dc.contributor.authorOzcan, Mete
dc.contributor.authorBulut, Ferah
dc.contributor.authorOrhan, Seval Ülkü
dc.date.accessioned2026-04-04T13:14:38Z
dc.date.available2026-04-04T13:14:38Z
dc.date.issued2024
dc.departmentİnönü Üniversitesi
dc.description.abstractAim: This study aims to investigate the potential neuroprotective effects of fibroblast growth factor-21 (FGF21) on dorsal root ganglion (DRG) neurons under high glucose (HG) conditions, mimicking diabetic neuropathy. Specifically, we hypothesize that FGF21 enhances cell viability and reduces glucose-induced neuronal death via the activation of the phosphatidyl-inositol-3-kinase (PI3K)/AKT signaling pathway. Materials and Methods: DRG neurons were cultured from 1-day-old to 2-day-old Wistar rats and exposed to HG concentrations to simulate diabetic conditions. Various concentrations of FGF21 were administered to the DRG neurons. Cell viability was assessed using the MTT assay (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide), a widely used enzymatic method for determining cellular metabolic activity. The involvement of the PI3K/AKT signaling pathway in mediating the effects of FGF21 was also examined through biochemical assays and pathway inhibitors. Results: Administration of FGF21 to DRG neurons exposed to HG conditions significantly protected cell viability and reduced glucose-induced neuronal death (p<0.05). The protective effects of FGF21 were found to be dose-dependent, with higher concentrations showing more pronounced benefits. Furthermore, the activation of the PI3K/AKT signaling pathway was confirmed to play a crucial role in the neuroprotective mechanism of FGF21, as inhibition of this pathway attenuated the protective effects. Conclusion: This study demonstrates for the first time that FGF21 has a neuroprotective effect on DRG neuron survival in a diabetic neuropathy model. By activating the PI3K/AKT signaling pathway, FGF21 helps maintain cell viability and reduces glucoserelated neuronal death. These findings provide a promising basis for the development of new therapeutic strategies for the treatment of diabetic neuropathy, leveraging the neuroprotective properties of FGF21.
dc.identifier.doi10.5455/annalsmedres.2024.06.111
dc.identifier.endpage610
dc.identifier.issn2636-7688
dc.identifier.issue8
dc.identifier.startpage605
dc.identifier.trdizinid1259108
dc.identifier.urihttps://doi.org/10.5455/annalsmedres.2024.06.111
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/1259108
dc.identifier.urihttps://hdl.handle.net/11616/107373
dc.identifier.volume31
dc.indekslendigikaynakTR-Dizin
dc.language.isoen
dc.relation.ispartofAnnals of Medical Research
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_TR_20250329
dc.subjectTıbbi Araştırmalar Deneysel
dc.subjectKlinik Nöroloji
dc.subjectNörolojik Bilimler
dc.subjectBiyoteknoloji ve Uygulamalı Mikrobiyoloji
dc.subjectHücre Biyolojisi
dc.titleFibroblast growth factor-21: Preserving cell viability in diabetic neuropathy through the AKT/PI3K cellular pathway
dc.typeArticle

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