The Study Of Toll-like Receptor4and Impaired Glucose Metabolism In Rat Adjuvant Induced Arthritis

Background and objectives:More and more studies show that rheumatoid arthritis and impaired glucosemetabolism such as insulin resistance, diabetes and pancreatic β-cell dysfunction areassociated. However, the possible mechanism of the rheumatoid arthritis associatedwith impaired glucose metabolism rarely reported. In this study, through theestablishment of the adjuvant-induced arthritis model in rats, from the perspective ofToll-4,we explore the possible mechanism of rheumatoid arthritis (RA) occurredimpaired glucose metabolism.Methods:The20SD rats were randomly divided into model group and normal controlgroups, the model group rats left hind foot plantar skin within0.1mL injection ofcomplete Freund’s adjuvant, normal control group of rats left rear foot plantar skin0.1mL saline injection, established the model after model15days, rats were killde atthe20days, tested fasting blood glucose, by ELISA tested rat serum fasting insulin,TNF-α levels; the pancreas tissue that was removed was detected the Toll receptor4expression by immunohistochemistry.Results:The left foot of the model group rats were swelling after first two days modeling,secondary joint swelling occured at13days, and the swelling were progressiveincreased.After modeling20days the rats were sacrificed. The fasting glucose levelsof the model group was higher than that of normal control group, the difference wassignificant (6.375±1.427mmol/L vs.5.388±0.987mmol/L，P <0.05); The fastinginsulin levels of the model group was lower than that of normal control group, thedifference was significant (9.892±1.674ng/ml vs.15.423±2.341ng/ml，P <0.05); TheserumTNF-α of the model group was higher than that of normal control group, thedifference was significant (4450.85±365pg/ml vs.2360.76±285pg/ml，P <0.05); theexpression of the Toll-4of the pancreatic islet in the Model group was higher thanthat of the pancreatic islet in the control group, the difference was statistically significant (P <0.05).Conclusions:Adjuvant-induced arthritis in rats appeared fasting glucose elevated, fastinginsulin decreased, the levels of the serum TNF-α elevated and the the expression ofToll-4of pancreas islet upregulated. The appearance of elevated fasting glucose maybe due to the expression of Toll-4of pancreas islet tissue upregulated and increasesleads to the activation of inflammatory pathways and dysfunction of pancreatic βcells, leading to reduction in fasting insulin secretion adjuvant-induced arthritis inrats.