Lactiplantibacillus plantarum 06CC2 upregulates intestinal ZO-1 protein and bile acid metabolism in Balb/c mice fed high-fat diet

• Published in: Bioscience of Microbiota, Food and Health Vol. 43; no. 1; pp. 13 - 22
• Main Authors: YAMASAKI, Masao, MIYAMOTO, Yuko, OGAWA, Kenjirou, NISHIYAMA, Kazuo, TSEND-AYUSH, Chuluunbat, LI, Yiran, MATSUSAKI, Tatsuya, NAKANO, Tomoki, TAKESHITA, Masahiko, ARIMA, Yuo
• Format: Journal Article
• Language: English
• Published: Tokyo BMFH Press 2024; Japan Science and Technology Agency
• Subjects: Accumulation; Adipose tissue; Bile; Bile acids; Cecum; Cholesterol; Clostridium; Clusters; Dairy products; Diet; Endotoxins; High fat diet; intestinal barrier; Intestine; Lactiplantibacillus plantarum; Lipid metabolism; Lipids; Lipopolysaccharides; Metabolism; Plasma; Protein turnover; Proteins; secondary bile acid; Zonula occludens-1 protein
• ISSN: 2186-3342; 2186-3342
• DOI: 10.12938/bmfh.2023-002

The effects of Lactiplantibacillus plantarum 06CC2 (LP06CC2), which was isolated from a Mongolian dairy product, on lipid metabolism and intestinal tight junction-related proteins in Balb/c mice fed a high-fat diet (HFD) were evaluated. The mice were fed the HFD for eight weeks, and the plasma and hepatic lipid parameters, as well as the intestinal tight junction–related factors, were evaluated. LP06CC2 slightly reduced the adipose tissue mass. Further, it dose-dependently decreased plasma total cholesterol (TC). The HFD tended to increase the plasma level of endotoxin and suppressed intestinal ZO-1 expression, whereas a low LP06CC2 dose increased ZO-1 expression and tended to reduce the plasma lipopolysaccharide level. Furthermore, a low LP06CC2 dose facilitated a moderate accumulation of Lactobacillales, a significant decrease in Clostridium cluster IV, and an increase in Clostridium cluster XVIII. The results obtained from analyzing the bile acids (BAs) in feces and cecum contents exhibited a decreasing trend for secondary and conjugated BAs in the low LP06CC2-dose group. Moreover, a high LP06CC2 dose caused excess accumulation of Lactobacillales and failed to increase intestinal ZO-1 and occludin expression, while the fecal butyrate level increased dose dependently in the LP06CC2-fed mice. Finally, an appropriate LP06CC2 dose protected the intestinal barrier function from the HFD and modulated BA metabolism.