Adamczyk-Grochala, JagodaKaniuka, OlenaDeręgowska, AnnaBandura, YuriiSabadashka, MariyaChala, DariyaKulachkovskyi, OlexandrKubis, HubertAdamczyk-Grochala, JagodaSybirna, Nataliia2024-11-122024-11-122024-09-2510.1016/j.bbadis.2024.167531https://rdb.ur.edu.pl/handle/item/52Raw data in a xlsx file: Original data used to generate the presentation of results in the figure 1-4.Endoplasmic reticulum stress, oxidative stress, and mitochondrial dysfunction are interconnected processes involved in the pathogenesis of diabetes mellitus (DM). In the present study, we demonstrate a distinct unfolded protein response (UPR) signaling pathways in two mammalian models of DM: β-TC-6 cell line and streptozotocin induced type 1 diabetes model in rats. However, a feature common to both systems was the upregulation of the GRP78 protein. Moreover, in vivo studies showed the disruption of the antioxidant system and an escalation of mitophagy against the background of a depletion of the level of ATP in pancreatic cells. In conclusion, we suggest that glucotoxic conditions induced GRP78 upregulation, and next cause depletion of the antioxidant pool and disruption of the functioning of antioxidant defense enzymes and in consequence promote mitophagy in pancreatic cells. Therefore, GRP78 may be considered as a potential therapeutic factor in patients with diabetes.enDiabetes mellitusEndoplasmic reticulum stressMitophagyOxidative stressGRP78raw dataset