发酵乳杆菌
氧化应激
促炎细胞因子
肠道菌群
加塞乳杆菌
乳酸菌
2型糖尿病
生物
葡萄糖稳态
炎症
植物乳杆菌
糖尿病
内分泌学
胰岛素抵抗
微生物学
内科学
乳酸
免疫学
生物化学
细菌
医学
遗传学
发酵
作者
Hainan Song,Hui Xue,Zeng Zhang,Jun Wang,Ao Li,Jiachao Zhang,Pengfei Luo,Zhan Meng,Xiaoli Zhou,Lihao Chen,Yajing Fang
标识
DOI:10.1021/acs.jafc.3c04665
摘要
This study aims to explore the preventive effects and underlying mechanisms of Lactobacillus fermentum CKCC1858 (CKCC1), L. fermentum CKCC1369 (CKCC2), Lactobacillus plantarum CKCC1312 (CKCC3), and Lactobacillus gasseri CKCC1913 (CKCC4) on high-fat diet combined with streptozotocin (HFD/STZ)-stimulated type 2 diabetes (T2D) in mice. Generally, the results indicated that most of the four probiotics reduced weight loss and liver and pancreas damage, significantly (p < 0.05) improved glucose metabolism by regulating glucagon-like peptide-1 (GLP-1), fasting glucose and insulin levels, and increasing expression of glucose transporters. Probiotics improved hyperlipemia, inflammation, and oxidative stress by reducing the secretion of blood lipids and proinflammatory cytokines, increasing antioxidant enzymes. Metagenomic results revealed that probiotics restored gut microbiota via enhancing (reducing) the relative abundance of beneficial bacteria (harmful bacteria) and altered specific metabolic pathways in T2D mice. CKCC1, CKCC3, and CKCC4 showed excellent effects compared to CKCC2. These results indicated that probiotics potentially prevented T2D, which is strain-specific.
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