Potential probiotics Lactobacillus casei K11 combined with plant extracts reduce markers of type 2 diabetes mellitus in mice

干酪乳杆菌 副干酪乳杆菌 益生菌 乳酸菌 生物 食品科学 化学 细菌 发酵 遗传学
作者
Ziheng Zhang,Lu Bai,Miaomiao Guan,Xihong Zhou,Xi Liang,Yan Lv,Huaxi Yi,Hui Zhou,T. Liu,Pimin Gong,Jing-Chao Sun,Lanwei Zhang
出处
期刊:Journal of Applied Microbiology [Wiley]
卷期号:131 (4): 1970-1982 被引量:11
标识
DOI:10.1111/jam.15061
摘要

Probiotics and plant extracts have been used to prevent the development of type 2 diabetes mellitus (T2DM). The study aimed to explore the effect of the interaction between potential probiotics and bitter gourd extract (BGE) or mulberry leaf extract (MLE) on T2DM.Potential probiotics were tested for their gastrointestinal tract viability and growth situation combined with BGE and MLE in vitro. The diabetes model was constructed in C57BL/6 mice, and the potential effect and mechanism of regulating blood glucose were verified. Hematoxylin-eosin staining (HE), gas chromatography (GC), ELISA, and RT-PCR were also used for analysis. The results showed that Lactobacillus casei K11 had outstanding gastrointestinal tract viability and growth situation with plant extracts. Administration of L. casei K11 combined with BGE and MLE significantly reduced blood glucose levels and ameliorated insulin resistance in diabetic mice than the administration of Lactobacillus paracasei J5 combined with BGE and MLE. Moreover, in L. casei K11 combined with BGE and MLE groups, lipid metabolism, oxidative stress, and proinflammatory cytokine levels were regulated. Furthermore, the results indicated that L. casei K11 combined with BGE and MLE improved free fatty acid receptor 2 (FFAR2) upregulation, glucagon-like peptide-1 (GLP-1) secretion, and short-chain fatty acid (SCFA) levels.These findings showed that L. casei K11 combined with BGE and MLE modified the SCFA-FFAR2-GLP-1 pathway to improve T2DM.This study identified a new modality for evaluating interactions between potential probiotics and plant extracts. Our findings revealed that L. casei K11 combined with BGE and MLE significantly promoted the SCFA-FFAR2-GLP-1 pathway to inhibit T2DM.
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