RESUMEN
<p><b>AIM</b>To observe the stability of BCG-induced insulin resistance model.</p><p><b>METHODS</b>The glucose tolerance, serum glucose, FFA, insulin, triglycerides, cholesterol, TNF-alpha and ALT level were measured. The change of GDR was measured by euglycemic clamp in model rats after given i.v. BCG 2, 4 and 8 weeks.</p><p><b>RESULTS</b>After 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 beta/alpha in pancreas increased. The serum levels of triglyceride, FFA and glucose were unchanged, but the level of serum TNF-alpha [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.</p><p><b>CONCLUSION</b>This novel model of immune insulin resistance is completely and constantly established.</p>