Naowaboot Jarinyaporn, Wannasiri Supaporn, Pannangpetch Patchareewan
Division of Pharmacology, Department of Preclinical Science, Faculty of Medicine, Thammasat University (Rangsit Campus), Pathum Thani, 12120, Thailand.
Division of Physiology, Department of Preclinical Science, Faculty of Medicine, Thammasat University (Rangsit Campus), Pathum Thani, 12120, Thailand.
J Physiol Biochem. 2016 Jun;72(2):269-80. doi: 10.1007/s13105-016-0477-5. Epub 2016 Mar 14.
Morin is a natural bioflavonoid that exhibits antioxidant and anti-inflammatory properties. The present study was designed to evaluate the effect of morin on insulin resistance, oxidative stress, and inflammation in a high-fat-diet (HFD)-induced obese mice. Obesity was induced in ICR mice by feeding a HFD (60 % kcal from fat) for 12 weeks. After the first 6 weeks, obese mice were treated with morin (50 or 100 mg/kg/day) once daily for further 6 weeks. Blood glucose, lipid profile, insulin, leptin, adiponectin, and markers of oxidative stress and inflammation were then measured. Liver was excised, subjected to histopathology, glycogen determination, and gene and protein expression analysis. Morin administration reduced blood glucose, serum insulin, leptin, malondialdehyde, interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) levels and increased serum adiponectin levels. Moreover, there was a reduction in serum lipid and liver triglyceride levels. Liver histology indicated that morin limited accumulation of lipid droplets. Interestingly, morin reduced expression of hepatic sterol regulatory element binding protein 1c (SREBP1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) and up-regulated hepatic carnitine palmitoyltransferase 1a (CPT1a) expression. Morin also stimulated glycogen storage and suppressed phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) protein expression. Furthermore, hepatic superoxide dismutase (SOD) and catalase (CAT) expression were increased after morin treatment. These findings indicate that morin has a positive effect in the HFD-induced obesity condition by suppressing lipogenesis, gluconeogenesis, inflammation, and oxidative stress activities.
桑色素是一种具有抗氧化和抗炎特性的天然生物类黄酮。本研究旨在评估桑色素对高脂饮食（HFD）诱导的肥胖小鼠胰岛素抵抗、氧化应激和炎症的影响。通过给ICR小鼠喂食HFD（脂肪提供60%的千卡热量）12周来诱导肥胖。在前6周后，肥胖小鼠每天接受一次桑色素（50或100毫克/千克/天）治疗，持续另外6周。然后测量血糖、血脂谱、胰岛素、瘦素、脂联素以及氧化应激和炎症标志物。切除肝脏，进行组织病理学检查、糖原测定以及基因和蛋白质表达分析。给予桑色素可降低血糖、血清胰岛素、瘦素、丙二醛、白细胞介素-6（IL-6）和单核细胞趋化蛋白-1（MCP-1）水平，并提高血清脂联素水平。此外，血清脂质和肝脏甘油三酯水平降低。肝脏组织学表明桑色素限制了脂滴的积累。有趣的是，桑色素降低了肝脏固醇调节元件结合蛋白1c（SREBP1c）、脂肪酸合酶（FAS）和乙酰辅酶A羧化酶（ACC）的表达，并上调了肝脏肉碱棕榈酰转移酶1a（CPT1a）的表达。桑色素还刺激糖原储存并抑制磷酸烯醇丙酮酸羧激酶（PEPCK）和葡萄糖-6-磷酸酶（G6Pase）蛋白表达。此外，桑色素治疗后肝脏超氧化物歧化酶（SOD）和过氧化氢酶（CAT）表达增加。这些发现表明，桑色素通过抑制脂肪生成、糖异生、炎症和氧化应激活动，对HFD诱导的肥胖状况具有积极作用。
