Published online Dec 15, 2023. doi: 10.4239/wjd.v14.i12.1824
Peer-review started: August 22, 2023
First decision: September 18, 2023
Revised: September 28, 2023
Accepted: November 25, 2023
Article in press: November 25, 2023
Published online: December 15, 2023
Processing time: 114 Days and 0.8 Hours
Fibroblast growth factor 21 (FGF21) plays a pivotal role in regulating glucose and lipid metabolism. Acute pancreatitis (AP) is a common inflammatory disease with clinical manifestations. Diabetes exacerbates intestinal permeability and intestinal inflammation, thus leading to the progression to AP. Our previous study indicated that FGF21 significantly attenuated susceptibility to AP in mice.
Yet, whether FGF21 similarly protects AP in diabetic mice remains unexplored.
Herein, we were intrigued to investigate the potential protective role of FGF21 against AP in diabetic mice.
In the present study, a mouse model of AP was established in db/db diabetic mice through ceruletide injections. By comparing the differences in AP indicators between diabetic mouse group (db), ceruletide-induced AP model group (AP), FGF21 treatment group (FGF21), and FGF21 combined with an antibiotic (Abx) cocktail treatment group (FGF21 + Abx), we investigated the protective effect of recombinant FGF21 protein and investigated whether FGF21 plays its role in the treatment of diabetic mice with AP by modulating the gut microbiota.
FGF21 notably diminished the levels of serum amylase, inflammatory factors and the histological evidence of inflammation in the pancreas and the small intestine in diabetic mice with AP. FGF21 also significantly altered the composition of the gut microbiota, reestablishing the Bacteroidetes/Firmicutes ratio. Upon treatment with an Abx cocktail to deplete the gut microbiota, the FGF21 + Abx group showed superior protective effect. The gut microbiota composition across different groups was further characterized, and a differential expression analysis of gene functions was undertaken using the PICRUSt2 prediction method. These findings suggested that FGF21 could potentially confer therapeutic effects on diabetic mice with AP by modulating the sulfate reduction I pathway and the superpathway of n-acetylceramide degradation in the gut microbiota.
This study reveals the potential of FGF21 in improving pancreatic and intestinal damage recovery, reducing blood glucose levels, and reshaping gut microbiota composition in diabetic mice with AP. Notably, the protective effects of FGF21 are augmented when combined with the Abx cocktail. These findings provide new insights into the prevention and treatment of diabetes complicated by AP.
Further investigation is required to elucidate the specific mechanisms by which the gut microbiota affects the protective effects of FGF21 against AP in diabetic mice.