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Beneficial Effects of Dietary Flaxseed Oil through Inflammation Pathways and Gut Microbiota in Streptozotocin-Induced Diabetic Mice.

Hui XiaYing WangXiangling ShiWang LiaoShaokang WangJing SuiGui-Ju Sun
Published in: Foods (Basel, Switzerland) (2023)
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% w / w FO feeding group (FO-L), and a diabetes with 10.5% w / w FO feeding group (FO-H) for six weeks. The 7.0% w / w and 10.5% w / w 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% w / w FO in diabetic mice. The 10.5% w / w 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% w / w and 10.5% w / w FO. FO feeding significantly attenuated hepatic LPS, TNF-α, and IL-1β levels. In addition, we observed that 7.0% w / w and 10.5% w / w 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.
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