The effects of chronic coffee exposure in models of type 2 diabetes mellitus (T2D) is scarcely studied, and the efficacy of the main coffee species has never been compared. We tested the hypothesis that long-term consumption of arabica and robusta coffee may differentially delay and affect T2D development in Zucker diabetic fatty rats. Three study groups received either chow mixed with arabica or robusta instant coffee (1.8% w/w) or unsupplemented chow food for 10 weeks. Both coffee species reduced liver triglyceride content and area under the curve of fasting and postprandial insulin. At study end, plasma adiponectin, total cholesterol and high density lipoprotein levels were higher in the robust group compared with both arabica and control groups. The liver gene expression of Glucose-6-phosphatase, catalytic subunit (G6pc) and Mechanistic target of rapamycin (mTOR) in robusta and Cpt1a in both coffee groups was downregulated. In conclusion, long-term consumption of both coffee species reduced weight gain and liver steatosis and improved insulin sensitivity in a rat model of T2D. Robusta coffee was seemingly superior to arabica coffee with respect to effects on lipid profile, adiponectin level and hepatic gene expression.
Background: Coffee consumption is inversely associated with type 2 diabetes. Cafestol, a bioactive compound in coffee, has demonstrated glucose-lowering and insulin-secretory properties in cell and animal studies. The acute effects of cafestol on glucose metabolism in humans have only been briefly investigated, and longer-term effects have not been explored. This study aimed to assess the effects of purified cafestol on insulin sensitivity and other metabolic parameters in healthy individuals with increased waist circumference at risk of developing type 2 diabetes. Methods: A 12-week randomized, placebo-controlled, parallel trial was conducted with 40 participants. Insulin suppression tests, mixed meal tests, and MRI scans were performed before and after the intervention. Results: Administering 6 mg of cafestol twice daily did not alter insulin sensitivity or glucose tolerance but led to significant reductions in body weight (2%), visceral fat volume (5%), and gamma-glutamyl transferase levels (15%) compared to the placebo. Conclusions: Cafestol may hold promise for weight and visceral fat reduction. Cafestol did not improve insulin sensitivity or glucose tolerance in this study but might still contribute to the observed inverse association between coffee consumption and type 2 diabetes. Future research should explore higher dosages and longer treatment durations, particularly in individuals with impaired glucose metabolism and type 2 diabetes.
Coffee consumption is associated with a reduced risk of Type-2 Diabetes. A bioactive compound in coffee, cafestol, has shown potential preventive effects for Type-2 Diabetes in cell and animal studies, but its potential benefits in humans have not been examined. In this randomized, double- blinded crossover intervention study, 15 healthy participants with increased waist circumference and thus elevated risk of developing Type-2 Diabetes underwent three oral glucose tolerance tests one week apart, with placebo, 7 mg- or 14 mg cafestol capsules ingested with the glucose load. There were no substantial differences in area under the curve (AUC) for glucose, insulin, glucagon-like peptide 1 (GLP-1) or gastric inhibitory peptide (GIP) on placebo or cafestol intervention study days. Among participants with impaired glucose tolerance and/or elevated fasting glucose (n=8, 53%), ingestion of 14 mg of cafestol resulted in an 11% larger AUC for GIP (p=0.046) and a 5% smaller AUC for glucose (p=0.14), compared to placebo. Our results suggest that cafestol may contribute to coffee's inverse association with risk of Type-2 Diabetes, particularly in subjects with impaired glucose tolerance, possibly through increased GIP secretion. Further studies are needed to confirm these novel findings in participants with impaired glucose metabolism, both after acute and longer-term cafestol intervention.