Obesity-associated inflammation is believed to promote metabolic dysregulation and insulin resistance. Colchicine has been well studied as an anti-inflammatory agent; however, its metabolic effects are not fully elucidated. We hypothesized that chronic intraperitoneal (IP) colchicine administration would improve inflammation and metabolic measures in high-fat diet fed mice.


8-week old C57BL/6 male mice were placed on a 45% fat diet for 8 weeks to induce obesity and inflammation. During weeks 12-16, mice were randomized to daily IP injections of colchicine 0.2mg/kg (high-dose [HD], n=14), 0.02mg/kg (low-dose [LD], n=12), or vehicle (V, n=11). Post-treatment, we measured serum hsCRP (ELISA) and body composition (DXA) as well as glucose levels during glucose and insulin tolerance tests (GTT, ITT) to assess glucose homeostasis.


Body fat% was not significantly different among HD, LD, and V (25.3±6.1% vs. 30.3±6.5% vs. 28.1±6.7%; p>.05). hsCRP was significantly decreased in the HD group (6.4±3.1µg/mL) vs. LD (10.0±1.4µg/mL; p<.01) and V (10.7±1.6µg/mL; p<.001). However, LD and V hsCRP were not significantly different (p>.05). 2-way ANOVA analysis of ITT glucose values revealed a significant (p<.05) group effect: HD AUC 670mg/dLxmin; LD 627mg/dLxmin; V 557mg/dLxmin. ITT glucose concentrations were statistically greater for HD vs. V from 60-120min (all ps<.01) and for HD vs. LD at 120min (p<.05). No group effect was observed for the GTT (p>.05).


4-weeks of IP colchicine at 0.2mg/kg, but not 0.02mg/kg, suppressed hsCRP, a marker of systemic inflammation in high-fat diet fed mice. However, our data suggest the 0.2mg/kg dose worsened whole-body insulin resistance, as evidenced by the ITT. Further studies are warranted to elucidate the metabolic effects of chronic IP colchicine administration in mice and to examine the metabolic effects of oral administration of colchicine.