Daily
coffee consumption is inversely associated with risk of type-2 diabetes (T2D).
Cafestol, a bioactive substance in
coffee, increases
glucose-stimulated insulin secretion in vitro and increases
glucose uptake in human skeletal muscle cells. We hypothesized that
cafestol can postpone development of T2D in KKAy mice. Forty-seven male KKAy mice were randomized to consume chow supplemented daily with either 1.1 (high), 0.4 (low), or 0 (control) mg of
cafestol for 10 weeks. We collected blood samples for fasting
glucose,
glucagon, and
insulin as well as liver, muscle, and fat tissues for gene expression analysis. We isolated islets of Langerhans and measured
insulin secretory capacity. After 10 weeks of intervention, fasting plasma
glucose was 28-30% lower in
cafestol groups compared with the control group (p < 0.01). Fasting
glucagon was 20% lower and
insulin sensitivity improved by 42% in the high-
cafestol group (p < 0.05).
Cafestol increased insulin secretion from isolated islets by 75-87% compared to the control group (p < 0.001). Our results show that
cafestol possesses
antidiabetic properties in KKAy mice. Consequently,
cafestol may contribute to the reduced risk of developing T2D in
coffee consumers and has a potential role as an
antidiabetic drug.