Published online Jun 7, 2023. doi: 10.3748/wjg.v29.i21.3280
Peer-review started: March 6, 2023
First decision: March 18, 2023
Revised: March 31, 2023
Accepted: May 8, 2023
Article in press: May 8, 2023
Published online: June 7, 2023
Processing time: 87 Days and 5 Hours
Bariatric surgery can significantly ameliorate type 2 diabetes mellitus (T2DM) through its rapid and durable weight-loss and hypoglycemic action. Both biles acids (BAs) and fibroblast growth factor (FGF) 15/19 are increased after surgery. Whether BAs and FGF15/19 participates in amelioration of T2DM after bariatric surgery and the underlying mechanism remain incompletely illuminated.
FGF15 which is induced by farnesoid X receptor (FXR) in ileum can improve the hepatic glucose metabolism through entero-hepatic circulation. Our previous study confirms that BA profiles within peripheral circulation and portal vein have changed after SG, with significant increase of FXR- activated BAs levels.
This study aimed to evaluate the effect of FGF15 on improvement of T2DM triggered by elevated BAs after sleeve gastrectomy (SG) and investigate the underlying mechanism.
The weight-loss and hypoglycemic action of SG were detected in a diabetic rat model induced by High-fat diet and streptozotocin (STZ), as well as the hepatic glycogen content and gluconeogenesis activity. Total BA (TBA) together with the FXR-agonistic BA subspecies levels in systemic serum and portal vein were examined at week 12 post-surgery. Then the expression and activity of ileal FXR and FGF15 and hepatic FGFR4 with its corresponding signal pathways involved in glucose metabolism were detected.
Compared with SHAM group, SG induced sustained weight loss and improved the hepatic glucose metabolism by promoting hepatic glycogen synthesis and inhibiting the gluconeogenesis. TBA levels and the FXR-agonistic subspecies in serum and portal vein were elevated after SG. Consequently, the ileal expression of FXR and FGF15 were also advanced. Moreover, the hepatic expression of FGFR4 and the activities of its corresponding pathways were stimulated in SG-operated rats.
FGF15, triggered by elevated BAs after SG, acts as an endocrine factor to induce the improvement of hepatic glucose metabolism through the intestine-liver crosstalk.
FXR-agonistic BA subspecies and FGF15 participate in improvement of hepatic glucose metabolism, and may be developed as new targets for the treatment of T2DM.