Abstract
Aim: There are many people with type 2 Diabetes Mellitus (T2DM) worldwide. Rouxen- Y Gastric Bypass (RYGB) is an effective surgery for treating T2DM with beneficial effects on β cell metabolism. However, the mechanism of how RYGB affects the pancreas, is not clear. We focused on metabolic changes in the pancreas of rats following RYGBand to investigate complex postoperative pancreatic metabolic reprogramming and to understand how RYGB improves islet function.
Methods: We performed RYGBonstreptozotocin-induced male T2DM rats. Then we measured indicators such as weight, fasting GLU, etc. After 10 weeks, pancreatic tissues were removed to identify and quantify differentially expressed proteins. Furthermore, functional analysis of these proteins and their associated pathways was conducted by bioinformatics methods.
Results: After surgery, 451 differentially expressed proteins associated with the mechanism ofRYGB were identified. Protein levels of regenerating islet-derived protein 3 (Reg3A), cell division cycle-associated protein 2 (CDCA2), and ADP-ribosylation factor 1 (Arf1) varied greatly, and Arf1 may be a point target in diabetes.
Conclusion: This research shows that RYGB could treat T2DM through changes in the pancreatic proteins. It will give some new insight into the molecular mechanism behind the effect of RYGB.
Keywords: T2DM, RYGB, proteomics, pancreatic protein, reg3A, CDCA2, Arf1.
Graphical Abstract
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