Abstract
Purpose
The purpose of this study was to investigate the regulatory effect of salidroside on the intestinal flora of mice with type 2 diabetes (T2DM) and its protective effect in the body.
Patients and Methods
We acclimated 8-week-old mice for 7 days, divided them into 4 groups, and continued dosing for 8 weeks. We recorded weekly blood glucose levels and body weight for each mouse. After the completion of the feeding cycle, the 16S rRNA of the intestinal flora in the mice was sequenced, and the insulin and C-peptide levels in each group of mice were measured. Four samples were taken from each group for liver and kidney section staining.
Results
Our results showed that gut microbiota diversity and function were significantly different between the diabetic mice and healthy mice and that insulin levels, body weight, and blood glucose levels could significantly influence gut microbiota changes at the genus level. The gut microbiota diversity and function of db/db mice were also altered after salidroside administration. Salidroside could attenuate inflammatory damage, lipid accumulation and inflammatory changes in the diabetic liver, as well as diabetic kidney damage. Candidatus arthromitus and Odoribacter are important species of the microbiota during diabetes and may serve as potential therapeutic targets.
Conclusion
Our investigation of the associated pathological conditions and fecal microbiota in db/db mice provides new insights into the pathogenesis of T2DM and provides implications for the diagnosis and treatment of T2DM.
Acknowledgments
Qin Zhao and Jing Shi should be considered co-first authors. This study was supported by Research Project of Sichuan Medical Association (S19072); Natural Science Foundation of Tibet Autonomous Region (XZ202101ZR0101G); Key Research Projects of Hospital of Chengdu Office of People’s Government of Tibetan Autonomous Region (Hospital.C.T.) (QH-1(2019)-03). The samples are stored in Biobank of Hospital of Chengdu Office of People’s Government of Tibetan Autonomous Region.
Disclosure
The authors report no conflicts of interest in this work.