Surfactin Mitigates a High-Fat Diet and Streptozotocin-Induced Type 2 Diabetes through Improving Pancreatic Dysfunction and Inhibiting Inflammatory Response

• Published in: International journal of molecular sciences Vol. 23; no. 19; p. 11086
• Main Authors: Chen, Xiaoyu, Zhao, Hongyuan, Lu, Yajun, Liu, Huawei, Meng, Fanqiang, Lu, Zhaoxin, Lu, Yingjian
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01-10-2022; MDPI
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Beta cells; Blood glucose; Body weight; Colon; Diabetes; Diabetes mellitus (non-insulin dependent); Endoplasmic reticulum; Fatty acids; Glucagon; Glucose; Glucose metabolism; gut-barrier; High fat diet; Homeostasis; Inflammation; Inflammatory response; Insulin; Insulin resistance; Insulin secretion; Intestinal microflora; Intestine; Liver diseases; Metabolism; Microbiota; Oxidative stress; Pancreas; Phosphatidylinositol kinase; Proteins; Rodents; Signal transduction; Streptozocin; Surfactin
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms231911086

Surfactin from Bacillus amyloliquefaciens fmb50 was utilized to treat mice with type 2 diabetes (T2DM) induced by a high-fat diet/streptozotocin (HFD/STZ). Our group’s earlier research indicated that surfactin could lower blood glucose and mitigate liver dysfunction to further improve HFD/STZ-induced T2DM through modulating intestinal microbiota. Thus, we further investigated the effects of surfactin on the pancreas and colon in mice with T2DM to elucidate the detailed mechanism. In the present study, mice with HFD/STZ-induced T2DM had their pancreatic and colon inflammation, oxidative stress, and endoplasmic reticulum stress (ERS) reduced when given oral surfactin at a dose of 80 mg/kg body weight. According to further research, surfactin also improved glucose metabolism by activating the phosphatidylinositol kinase (PI3K)/protein kinase B (Akt) signaling pathway, further protecting islets β-cell, promoting insulin secretion, inhibiting glucagon release and mitigating pancreas dysfunction. Additionally, after surfactin treatment, the colon levels of the tight junction proteins Occludin and Claudin-1 of T2DM mice were considerably increased by 130.64% and by 36.40%, respectively. These findings revealed that surfactin not only ameliorated HFD/STZ-induced pancreas inflammation and dysfunction and preserved intestinal barrier dysfunction and gut microbiota homeostasis but also enhanced insulin sensitivity and glucose homeostasis in T2DM mice. Finally, in the further experiment, we were able to demonstrate that early surfactin intervention might delay the development of T2DM caused by HFD/STZ, according to critical biochemical parameters in serum.