ESTABLISHMENT OF IMMUNE INSULIN RESISTANCE MODEL IN THE RATS BY IV INJECTION OF BCG

AIMTo observe the stability of BCG-induced insulin resistance model. METHODSThe glucose tolerance, serum glucose, FFA, insulin, triglycerides, cholesterol, TNF-α and ALT level were measured. The change of GDR was measured by euglycemic clamp in model rats after given iv BCG 2, 4 and 8 weeks. RESULTSAfter 2, 4 and 8 weeks, the GIR and glucose tolerance of the animals deceased significantly. After 2, 4 and 8 weeks, BCG infusion resulted in a pronounced reduction in glucose tolerance and insulin-stimulated glucose disposal rate ［GDR=GDR: (29±6) vs (13±7) mg·kg^-1·min^-1 2 weeks; (29±6) vs (11±7) mg·kg^-1·min^-1 4 weeks and (23±3) vs (16±3) mg·kg^-1·min^-1 8 weeks, respectively, P<0.01］. BCG infusion resulted in a pronounced increase in the weights of the liver ［(6.2±0.9) vs (8.2±1.3) g, P<0.05］ and spleens ［(0.51±0.11) vs (1.4±0.4) g, P<0.01］. The histo-pathological results showed that BCG infusion resulted severe inflammation in the livers and spleens and the ratio of β/α in pancreas increased. The serum levels of triglyceride, FFA and glucose were unchanged, but the level of serum TNF-α ［(543±60) vs (759±137) pg·mL^-1, P<0.05］ and insulin ［(31±5) vs (36±5) mu·L^-1, P>0.05］ increased. CONCLUSIONThis novel model of immune insulin resistance is completely and constantly established.