Xia Hui, Wang Ying, Shi Xiangling, Liao Wang, Wang Shaokang, Sui Jing, Sun Guiju
Key Laboratory of Environmental Medicine and Engineering of Ministry of Education, Department of Nutrition and Food Hygiene, School of Public Health, Southeast University, Nanjing 210009, China.
Research Institute for Environment and Health, Nanjing University of Information Science and Technology, Nanjing 211544, China.
Foods. 2023 Aug 28;12(17):3229. doi: 10.3390/foods12173229.
Flaxseed oil (FO) has displayed potential anti-diabetes properties by providing a high content of α-linolenic acid. However, the effects and mechanisms of FO on type 1 diabetes are still unclear. The present study aims to explore the effects of different doses of FO feeding on hepatic inflammation and gut microbiota in streptozotocin-induced diabetic mice. Forty-eight six-week-old C57BL/6J male mice were divided into a control group (CON), a diabetic group (MOD), a diabetes with 7.0% / FO feeding group (FO-L), and a diabetes with 10.5% / FO feeding group (FO-H) for six weeks. The 7.0% / and 10.5% / FO feeding groups exhibited potential recovery of the number and size of pancreas tissues. The fasting blood glucose level was significantly decreased only after 4 weeks of feeding with 10.5% / FO in diabetic mice. The 10.5% / FO feeding group significantly decreased the postprandial blood glucose level of mice in the OGTT test. Hepatic glycogen levels were dramatically upregulated in the mice fed with both 7.0% / and 10.5% / FO. FO feeding significantly attenuated hepatic LPS, TNF-α, and IL-1β levels. In addition, we observed that 7.0% / and 10.5% / FO feedings notably downregulated hepatic gene and protein expressions of TLR4, MyD88, and P65. Furthermore, only 10.5% FO regulated fecal microbiota by increasing the relative abundance of the Bacteroidetes phylum, Lactococcus family, and Muribaculaceae and Streptococcaceae family and genus in streptozotocin-induced diabetic mice. Therefore, we conclude that FO feeding plays a role in anti-inflammation via the regulation of hepatic LPS/TLR4/MyD88 pathways and gut microbiota. In addition, different doses of FO supplementation may exhibit varying mechanisms in streptozotocin-induced mice.
亚麻籽油(FO)因其富含α-亚麻酸而显示出潜在的抗糖尿病特性。然而,FO对1型糖尿病的影响和机制仍不清楚。本研究旨在探讨不同剂量的FO喂养对链脲佐菌素诱导的糖尿病小鼠肝脏炎症和肠道微生物群的影响。将48只六周龄的C57BL/6J雄性小鼠分为对照组(CON)、糖尿病组(MOD)、7.0%/FO喂养的糖尿病组(FO-L)和10.5%/FO喂养的糖尿病组(FO-H),持续六周。7.0%/和10.5%/FO喂养组的胰腺组织数量和大小有潜在的恢复。仅在糖尿病小鼠用10.5%/FO喂养4周后,空腹血糖水平显著降低。在口服葡萄糖耐量试验中,10.5%/FO喂养组显著降低了小鼠的餐后血糖水平。用7.0%/和10.5%/FO喂养的小鼠肝脏糖原水平显著上调。FO喂养显著降低了肝脏脂多糖、肿瘤坏死因子-α和白细胞介素-1β水平。此外,我们观察到7.0%/和10.5%/FO喂养显著下调了肝脏中Toll样受体4、髓样分化因子88和P65的基因和蛋白表达。此外,仅10.5%的FO通过增加链脲佐菌素诱导的糖尿病小鼠中拟杆菌门、乳球菌科以及毛螺菌科和链球菌科及其属的相对丰度来调节粪便微生物群。因此,我们得出结论,FO喂养通过调节肝脏脂多糖/Toll样受体4/髓样分化因子88通路和肠道微生物群发挥抗炎作用。此外,不同剂量的FO补充在链脲佐菌素诱导的小鼠中可能表现出不同的机制。