诱导型2型糖尿病大鼠肝磷脂水平的追踪及恩帕列净对其水平的影响。

Riyam Bassil Ali, Majid Hameed Ahmed, Haidar K Ibrahim, Hasanain Sh Mahmood
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引用次数: 0

摘要

背景:Hepcidin是一种促进铁稳态的激素,可通过肝脏或肝外途径产生。它的产生可能受到巨噬细胞释放的促炎介质的影响,这些促炎介质在外周胰岛素抵抗的发展中起作用。胰岛素本身可增加胰腺β细胞产生的肝磷脂激素。目的:探讨诱导2型糖尿病(T2DM)对白化wister大鼠hepcidin水平的影响。此外,为了研究与对照组相比,使用2周的钠-葡萄糖共转运蛋白2抑制剂(SGLT2抑制剂)恩帕列净对hepcidin水平的影响。方法:采用介入性研究方法,将36只大鼠随机分为3组(A:阴性对照组,B:阳性对照组,C:恩帕列净组)。两只大鼠因不同的原因被排除在研究之外。采用高脂/高糖饮食(HFD/HSD)诱导T2DM 8周。然后以35 mg/kg/天的剂量给予C组恩帕列净2周。在基线、第8周和第10周间隔时测定Hepcidin水平。采用酶联免疫吸附法(ELISA)测定Hepcidin。结果:B组和C组诱导T2DM后Hepcidin水平均显著升高。HFD/HSD停药2周后,B组Hepcidin水平无显著降低,c组Hepcidin水平显著降低。A组第10周Hepcidin水平与基线比较无统计学差异。结论:T2DM的诱发与hepcidin水平的显著升高有关。依帕列净显著降低新造糖尿病大鼠肝磷脂水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tracking hepcidin level in induced type 2 diabetic rats and how Empagliflozin affects its level.

Background: Hepcidin is a hormone that contributes to iron homeostasis, produced either through hepatic or extrahepatic pathways. Its production may be affected by proinflammatory mediators released by macrophages, which play a role in the development of peripheral insulin resistance. Insulin itself may increase the production of hepcidin hormone from pancreatic β-cells.

Objectives: To evaluate the impact of induction of type 2 diabetes mellitus (T2DM) in albino wister rats on the level of hepcidin. Also, to examine the role of 2-week use of Empagliflozin, a sodium-glucose cotransporter-2 inhibitor (SGLT2 Inhibitor), on the hepcidin level comparing to control.

Method: An interventional study includes randomization of 36 rats into three groups (A: negative control, B: positive control, and C: Empagliflozin group). Two rats were excluded from the study for different reasons. T2DM was induced using high-fat diet/high-sugar diet (HFD/HSD) for 8 weeks. Empagliflozin was then given to Group C for 2 weeks at a dose of 35 mg/kg/day. Hepcidin level was determined at the baseline, and at week 8 and week 10 intervals. Hepcidin was determined using enzyme-linked immunosorbent assay (ELISA).

Results: Hepcidin level significantly increased following the induction of T2DM in both B and C Groups. Hepcidin level in Group B insignificantly reduced 2 weeks after discontinuation of HFD/HSD and significantly reduced in Group C. Group A experienced no statistical difference in hepcidin level at week 10 when compared to baseline.

Conclusion: Induction of T2DM is associated with a significant increase in the level of hepcidin. Empagliflozin significantly reduced hepcidin level in newly induced diabetic rats.

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