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獐芽菜苦苷补充剂可预防高脂饮食诱导的肥胖相关慢性炎症和胰岛素抵抗。

Swertiamarin supplementation prevents obesity-related chronic inflammation and insulin resistance in mice fed a high-fat diet.

机构信息

School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou Zhejiang, China.

Key Laboratory of Laboratory Medicine, Ministry of Education, Wenzhou Medical University, Wenzhou Zhejiang, China.

出版信息

Adipocyte. 2021 Dec;10(1):160-173. doi: 10.1080/21623945.2021.1906510.

Abstract

Obesity is characterized by low-grade chronic inflammation, which underlies insulin resistance and non-alcoholic fatty liver disease (NAFLD). Swertiamarin is a secoiridoid glycoside that has been reported to ameliorate diabetes and NAFLD in animal models. However, the effects of swertiamarin on obesity-related inflammation and insulin resistance have not been fully elucidated. Thus, this study investigated the effects of swertiamarin on inflammation and insulin resistance in high-fat diet (HFD)-induced obese mice. C57BL/6 mice were fed a HFD or HFD containing swertiamarin for 8 weeks. Obesity-induced insulin resistance and inflammation were assessed in the epididymal white adipose tissue (eWAT) and livers of the mice. Swertiamarin attenuated HFD-induced weight gain, glucose intolerance, oxidative stress, and insulin resistance, and enhanced insulin signalling in mice. Compared to HFD-fed mice, the swertiamarin-treated mice exhibited increased lipolysis and reduced adipocyte hypertrophy and macrophage infiltration in eWAT. Moreover, swertiamarin alleviated HFD-mediated hepatic steatosis and inflammation by suppressing activation of the p38 MAPK and NF-κB pathways within the eWAT and liver of obese mice. In conclusion, supplementation with swertiamarin attenuated weight gain and hepatic steatosis, and alleviated obesity-associated inflammation and insulin resistance, in obese mice.

摘要

肥胖的特征是低度慢性炎症,这是胰岛素抵抗和非酒精性脂肪性肝病(NAFLD)的基础。獐牙菜苦苷是一种裂环烯醚萜类糖苷,据报道它可以改善动物模型中的糖尿病和 NAFLD。然而,獐牙菜苦苷对肥胖相关炎症和胰岛素抵抗的影响尚未完全阐明。因此,本研究探讨了獐牙菜苦苷对高脂肪饮食(HFD)诱导肥胖小鼠炎症和胰岛素抵抗的影响。C57BL/6 小鼠喂食 HFD 或 HFD 加獐牙菜苦苷 8 周。评估了肥胖诱导的胰岛素抵抗和炎症在附睾白色脂肪组织(eWAT)和肝脏中的小鼠。獐牙菜苦苷减轻了 HFD 诱导的体重增加、葡萄糖不耐受、氧化应激和胰岛素抵抗,并增强了小鼠的胰岛素信号转导。与 HFD 喂养的小鼠相比,獐牙菜苦苷处理的小鼠表现出脂肪分解增加,脂肪细胞肥大和巨噬细胞浸润减少。此外,獐牙菜苦苷通过抑制肥胖小鼠 eWAT 和肝脏中 p38 MAPK 和 NF-κB 途径的激活,减轻了 HFD 介导的肝脂肪变性和炎症。总之,獐牙菜苦苷的补充减轻了肥胖小鼠的体重增加和肝脂肪变性,并缓解了肥胖相关的炎症和胰岛素抵抗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a416/8023247/b569adfeea81/KADI_A_1906510_F0001_OC.jpg

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