| Authors | reza bayat |
| Conference Title | سومین کنگره بین المللی علوم ازمایشگاهی2024 |
| Holding Date of Conference | 2024-02-15 - 2024-02-18 |
| Event Place | 1 - تهران |
| Presented by | دانشگاه تهران |
| Presentation | SPEECH |
| Conference Level | International Conferences |
Abstract
Introduction
Type 2 diabetes is a metabolic disorder in which the inability to regulate glucose levels is evident, which is caused by the resistance of cells to insulin and insulin. Improper eating habits and inactivity are mentioned. This disease is becoming a global problem, with the number of people suffering from this disease reaching 592 million in 2035. Useful food is formed, which is caused by many factors and is associated with disruption in the production of its metabolites Studies show that this disorder in the intestinal barrier can affect insulin resistance by changing the signaling and metabolic pathways.
Methods
In this study, the emphasis on the importance of the issue of diabetes and the effect of the gut microbiome on this disease has been investigated, in this direction, articles and reliable research sources such as Google Scholar, PubMed and Science Direct have been used
Results
The results indicate that probiotics can be effective in preventing and even treating type 2 diabetes. By increasing the sensitivity of cells to insulin, probiotics reduce blood glucose and glycosylated hemoglobin. Observations show that probiotic metabolites in the intestine can be associated with an increase in insulin secretion and a decrease in glucagon, which helps to reduce blood glucose in diabetics
Conclusions
The obtained results show that the metabolite of probiotics living in the intestine by producing short-chain fatty acids such as butyrate reduces inflammatory factors that can have anti-diabetic effects. These fatty acids, by activating multiple mechanisms, increase the insulin hormone and increase the sensitivity of cells. Increases liver and muscle to insulin through GLUT4. Decreasing a group of intestinal probiotics increases plasma lipopolysaccharide, which can accelerate pancreatic beta cell apoptosis and cause hyperglycemia.