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首页> 外文期刊>Endocrine journal >Liraglutide prevents diabetes progression in prediabetic OLETF rats
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Liraglutide prevents diabetes progression in prediabetic OLETF rats

机译：利拉鲁肽可预防糖尿病前期OLETF大鼠的糖尿病进展

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References(43) Cited-By(8) One of human GLP-1 analogues, liraglutide has been approved as adjuvant therapy to oral medication in T2DM. It was also shown to prevent diabetes in obese subjects and rats. However, it is unknown whether liraglutide can effectively mitigate the effects of prediabetes. We therefore investigate this by treating 12-weeks old Otsuka-Long-Evans-Tokushima fatty (OLETF) rats with liraglutide 50, 100, and 200 μg/kg, respectively twice a day for 12 weeks. Eight Long-Evans-Tokushima-Otsuka (LETO) rats with saline injection served as normal controls. Body weight, food intake, lipid profiles, inflammatory markers (fibrinogen, Hs-CRP, IL-6, TNFα, and PAI-1), glycemic metabolism and insulin sensitivity, and apoptotic factors (Bcl-2 and Bax) expression were monitored. We found that 12-week old OLETF rats had significantly increased body weight, food intake, serum levels of lipid profiles, inflammatory markers, and insulin compared to LETO rats. FPG level was significantly increased but still lower than 7mmol/L without impaired glucose tolerance (IGT). After 12 weeks, vehicle-treated OLETF rats had further deterioration in IFG, IGT, insulin resistance, lipid profiles, and inflammatory state. Pancreatic islets were hypertrophic with distorted structure, scarring, and inflammatory cell infiltration. However, in the three liraglutide-treated groups, IFG, IGT, the increased lipid profiles and inflammatory markers were reversed. Insulin resistance was similar to the level before the treatment. Moreover, liraglutide restored the islet structure, up-regulated Bcl-2 expression and down-regulated Bax expression. It indicated that liraglutide could suppress diabetes onset in OLETF rats with prediabetes, probably by reserving β cell function via regulating apoptotic factors as well as ameliorating lipid metabolism and inflammatory reactions.
机译：参考文献（43）Cited-By（8）利拉鲁肽是人类GLP-1类似物之一，已被批准作为T2DM中口服药物的辅助疗法。它也显示可以预防肥胖受试者和大鼠的糖尿病。然而，利拉鲁肽是否能有效减轻前驱糖尿病的影响尚不清楚。因此，我们通过每天两次分别用利拉鲁肽50、100和200μg/ kg处理12周大的Otsuka-Long-Evans-Tokushima脂肪（OLETF）大鼠来进行调查，持续12周。八只注射盐水的Long-Evans-Tokushima-Otsuka（LETO）大鼠作为正常对照。监测体重，食物摄入量，脂质分布，炎性标志物（纤维蛋白原，Hs-CRP，IL-6，TNFα和PAI-1），糖代谢和胰岛素敏感性以及凋亡因子（Bcl-2和Bax）的表达。我们发现，与LETO大鼠相比，12周龄的OLETF大鼠的体重，食物摄入量，血清脂质水平，炎性标志物和胰岛素水平显着增加。 FPG水平显着升高，但仍低于7mmol / L，而葡萄糖耐量（IGT）并未受损。 12周后，用载体治疗的OLETF大鼠的IFG，IGT，胰岛素抵抗，脂质分布和炎症状态进一步恶化。胰岛肥大，结构扭曲，瘢痕形成和炎性细胞浸润。但是，在三个利拉鲁肽治疗组IFG，IGT中，脂质分布和炎症标志物的增加被逆转。胰岛素抵抗与治疗前相似。此外，利拉鲁肽恢复了胰岛结构，Bcl-2表达上调和Bax表达下调。这表明利拉鲁肽可能通过调节凋亡因子以及改善脂质代谢和炎症反应来保留β细胞功能，从而抑制糖尿病前期OLETF大鼠的糖尿病发作。

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