Objective: Epidemiological evidence shows that chronic coffee consumption in humans is correlated with a lower incidence of type 2 diabetes mellitus. For the experimental exploration of the underlying mechanisms, this effect needs to be replicated in an animal model of type 2 diabetes with a short lifespan.
Design: Male C57BL/6 mice consumed regular coffee or water ad libitum and the development of obesity and diabetes caused by high-fat diet (55% lipids, HFD) was observed from week 10 on for 35 weeks in comparison with mice feeding on a defined normal diet (9% lipids, ND).
Results: The massive weight gain in HFD mice was dose-dependently retarded (P=0.034), the moderate weight gain in ND mice was abolished (P<0.001) by coffee consumption, probably because of a lower feeding efficiency. The consumption of fluid (water or coffee) was significantly diminished by HFD (P<0.001), resulting in a higher coffee exposure of ND mice. On week 21 intraperitoneal glucose tolerance tests (IPGTT) showed a dose-dependent faster decline of elevated glucose levels in coffee-consuming HFD mice (P=0.016), but not in ND mice. Remarkably, a spontaneous decrease in non-fasting glycaemia occurred after week 21 in all treatment groups (P<0.001). On week 39 the IPGTT showed diminished peak of glucose levels in coffee-consuming HFD mice (P<0.05). HFD mice were hyperinsulinaemic and had significantly (P<0.001) enlarged islets. Coffee consumption did not affect islet size or parameters of beta-cell apoptosis, proliferation and insulin granule content.
Conclusion: Coffee consumption retarded weight gain and improved glucose tolerance in a mouse model of type 2 diabetes and corresponding controls. This gives rise to the expectation that further insight into the mechanism of the diabetes-preventive effect of coffee consumption in humans may be gained by this approach.