Department of Modern Technologies of Medical Diagnostics and Treatment, Bogomoletz National Medical University, Kyiv 03115, Ukraine.
Department of Biochemistry of Vitamins and Coenzymes, Palladin Institute of Biochemistry, Kyiv 01054, Ukraine.
Endocr Metab Immune Disord Drug Targets. 2024;24(11):1335-1345. doi: 10.2174/0118715303273125231121062111.
Effects of propionic acid (PA) on the cellular and molecular processes in the small intestine under type 2 diabetes mellitus (T2DM)-induced endoplasmic reticulum (ER) stress remain incompletely studied.
The aim of the study was to assess the state of unfolded protein response (UPR) system in the small intestine of diabetic rats and to explore PA's influence on metformin treatment.
Male Wistar rats were divided into 1) control and 2) T2DM groups, and groups receiving (14 days, orally) 3) metformin (60 mg/kg), 4) PA (60 mg/kg), and 5) PA+metformin. Western blotting, RT-PCR, and transmission electron microscopy were performed.
We found that T2DM induced elevation of ER intermembrane space and UPR overactivation based on increased GRP78, ATF6 and PERK levels in small intestine. Metformin treatment led to a further UPR activation. PA supplementation partially restored enterocytes functioning via normalization of ATF6 and PERK content, while IRE1 level reached the maximum value, compared to all groups. The most pronounced effect of adaptation to the T2DMinduced ER stress was observed after combined metformin and PA action. In particular, decreased ER intermembrane space in enterocytes was detected compared to separate metformin and PA administration, which was accompanied by restored GRP78, PERK and IRE1 levels.
Our study proves the safety of additional therapy with propionic acid in combination with metformin for the functional state of small intestine. Due to its ability to modulate UPR signaling, PA may be considered a safe and perspective candidate for supportive therapy in T2DM, especially for neuroprotection.
丙酸(PA)对 2 型糖尿病(T2DM)诱导的内质网(ER)应激下小肠细胞和分子过程的影响尚未完全研究清楚。
本研究旨在评估糖尿病大鼠小肠 unfolded protein response(UPR)系统的状态,并探讨 PA 对二甲双胍治疗的影响。
雄性 Wistar 大鼠分为 1)对照组和 2)T2DM 组,接受 3)二甲双胍(60mg/kg)、4)PA(60mg/kg)和 5)PA+二甲双胍治疗(14 天,口服)。进行 Western blot、RT-PCR 和透射电子显微镜检查。
我们发现,T2DM 诱导的小肠 ER 间隙增加和 UPR 过度激活,表现为 GRP78、ATF6 和 PERK 水平升高。二甲双胍治疗导致 UPR 进一步激活。PA 补充部分通过恢复 ATF6 和 PERK 含量来恢复肠细胞功能,而 IRE1 水平达到所有组中的最大值。与单独使用二甲双胍和 PA 相比,联合使用二甲双胍和 PA 对适应 T2DM 诱导的 ER 应激的作用最为明显。特别是,与单独使用二甲双胍和 PA 相比,进入细胞的 ER 间隙减小,同时 GRP78、PERK 和 IRE1 水平得到恢复。
我们的研究证明了在二甲双胍治疗的基础上联合使用丙酸进行额外治疗对小肠功能状态的安全性。由于其调节 UPR 信号的能力,PA 可能被认为是 T2DM 支持治疗的一种安全且有前景的候选药物,特别是在神经保护方面。