Plasma trimetylamino N-oxide levels in rats with experimental diabetes induced HİGH fatty diet and streptozotocin enriched by phosphatidyl choline

The aim of this study was to investigate the relationship between TMAO, the level of which is increased in the intestinal flora by high fat and phosphatidylcholine-rich diet, and Type 2 Diabetes. In the study, 36 rats weighing 250±20 grams were divided into 6 groups. Control group fed with basal diet (Group 1), high fat diet (Group 2), phosphatidylcholine rich high fat diet (Group 3), phosphatidylcholine rich high fat diet+spreptozotocin (STZ) (Group 4), TMAO, LPS, CRP, IL-10, IL-6, TNF-alpha, IL 1beta levels and other biochemical parameters were studied in the blood samples taken after the rats were fed with phosphatidylcholine rich high fat diet+spreptozotocin+SFN (Group 5) and phosphatidylcholine rich high fat diet+spreptozotocin+DMB (Group 6) for 13 weeks. There was no significant difference between Group 1 and Group 2 in terms of TMAO levels (p<0.05). In Group 3, TMAO levels increased significantly compared to Group 1 and Group 2 (p<0.05).In Group 4, TMAO levels and glucose levels increased almost at the same rate. In this group, CRP, IL-1Beta, IL-6, TNF-alpha and LPS levels were higher while IL-10 levels were lower (p<0.001). After treatment with SFN and DMB, TMAO, glucose, LPS, TNF-alpha, IL-6, IL-1Beta levels decreased. The liver was examined histologically and immunohistologically and it was observed that steatosis, fibrosis, ballooning and inflammation cells increased in Groups 2 and 3. In the treatment groups (Group 5 and Group 6), there was a decrease in steatosis and fibrosis formation in the liver. In conclusion, elevated TMAO levels induced by high-fat and phosphatidyl choline-rich diet and flora increase plasma LPS and CRP, IL-1Beta, IL-6, TNF-alpha levels. This is because TMAO, an inflammatory metabolite, inhibits glucose uptake and prevents glucose entry into the cell. In addition, TMAO and LPS and CRP, IL-1Beta, IL-6, TNF-alpha levels decreased with SFN and DMB treatment. We think that HFD and dietary types that create TMAO in the intestinal flora may cause diabetes by increasing the levels of both TMAO and inflammatory cytokines and normalizing TMAO levels in diabetics may be a treatment option in the future. Keywords: Gut microbiota, TMAO, Inflammatory cytokines.