Published online Apr 15, 2021. doi: 10.4239/wjd.v12.i4.453
Peer-review started: December 11, 2020
First decision: December 31, 2020
Revised: January 13, 2021
Accepted: March 7, 2021
Article in press: March 7, 2021
Published online: April 15, 2021
Processing time: 118 Days and 20.1 Hours
Type 2 diabetes mellitus is one of the important complications of obesity. Bariatric surgery can treat obesity and diabetes effectively, but the recurrence of diabetes after surgery is still one of the problems to be solved. However, whether oligofructose has an effect on metabolism after bariatric surgery remains to be further studied.
Prebiotics promote the weight loss and improve the metabolism of glucose and lipid. The mechanism of these benefits may be due to reduced energy intake, regulation of gut microbiota, improvement of low-grade inflammation, and increase of intestinal hormones, such as glucagon like peptide-1 (GLP-1) and peptide YY, which prompted us to explore whether prebiotics can reduce or delay the recurrence of diabetes after surgery.
The present study aimed to find the effect and mechanism of oligofructose on diabetic remission in diabetic rats after sleeve gastrectomy (SG).
SG and SHAM operation were performed on diabetes rats induced with a high-fat diet (HFD), nicotinamide, and low-dose streptozotocin. Then the rats in SHAM and SG groups were continuously provided with the HFD, and the rats in the SG-oligofructose group were provided with a specific HFD containing 10% oligofructose. Body weight, calorie intake, oral glucose tolerance test, homeostasis model assessment of insulin resistance, lipid profile, serum insulin, GLP-1, total bile acids, lipopolysaccharide (LPS), and colonic microbiota levels were determined and compared at the designated time points. All statistical analyses was performed using Solutionsstatistical Package for the Social Sciences version 19.0 (IBM, United States), and the statistically significant difference was considered at P < 0.05.
Oligofructose treatment reduced body weight, energy intake, and LPS levels, increased GLP-1 levels, and improved insulin resistant and lipid profiles. Oligofructose also altered the gut microbiota in the SG-oligofructose group.
Oligofructose partially prevents HFD-induced glucose and lipid metabolism damage after SG in rats, and the effects of oligofructose on calorie intake, insulin, GLP-1, LPS, and gut microbiota may contribute to protective function for damaged metabolism.
The results of this study provide evidence that oligofructose could be a promising agent for the treatment in diabetic rats after SG. Further studies that assess the effect of oligofructose on the mechanism of preventing HFD-induced glucose and lipid metabolism damage after SG may substantiate our findings and pave the path for clinical translation of the therapeutic effects of oligofructose.