Modest decreases in 2-hour glucose and AUC glucose were observed after a 16-week consumption of 5 cups of caffeinated instant coffee per day. A consumption of decaffeinated coffee did not show such decreases. However, waist circumference decreased in the caffeinated coffee group and increased in the decaffeinated coffee group. With allowance for the change in waist circumference, the postload glucose levels seemed to be lowered after a 16-week consumption of caffeinated or decaffeinated coffee.
The differential change in waist circumstance between the caffeinated and decaffeinated groups was indeed problematic. An apparent increase in waist circumference after a 16-week consumption of decaffeinated coffee was ascribed partly to a decrease in physical activity as reported by 3 men. In the caffeinated coffee group, physical activity did not reportedly change to such an extent, but slight decreases in body weight and waist circumference may have been due to an unreported change in diet or physical activity. The decreases in body weight and waist circumference in the caffeinated coffee group may be regarded as compatible with caffeine's effects of increasing thermogenesis and fat oxidation [29
]. In a meta-analysis of chamber studies on humans [30
], a dose of 300
mg/day of caffeine was associated with an 80
kcal increase of energy expenditure per day. Caffeine enhances the release of epinephrine and free fatty acids in a fasting condition [6
], and these physiological effects may be linked to the increase in energy expenditure [29
]. However, it remains uncertain whether a long-term use of caffeine is beneficial in maintaining body weight or decreasing body fat, while an increase in caffeine intake was reported to be associated with a small reduction in long-term weight in an observational study [31
The present study suggested that both caffeinated and decaffeinated coffee were associated with a modest improvement in the 2-hour glucose concentrations. The present findings are consistent with the results from observational studies [32
]. These studies consistently showed that coffee consumption was more strongly associated with lower concentrations of 2-hour glucose than of fasting glucose during a 75
g OGTT [32
]. The present study adds to evidence that coffee compounds other than caffeine are protective in glucose metabolism. Chlorogenic acids and other noncaffeine coffee compounds may exert protective effects by decreasing hepatic glucose production through inhibition of hepatic glucose-6-phosphate translocase [34
], delaying intestinal glucose absorption as suggested by an altered profile of plasma concentrations of gastrointestinal hormones [35
], and increasing whole-body glucose disposal or insulin sensitivity [36
]. Coffee polyphenols were also shown to be protective against the damage of pancreatic islet caused by oxidative stress [37
There is no doubt that caffeine or caffeinated coffee deteriorates glucose tolerance when administered prior to glucose load or meal. This adverse effect was observed not only in healthy subjects [6
] but also in patients with type 2 diabetes mellitus [7
], with a habitual consumption of caffeinated coffee of different types. The caffeine's acute effect on glucose tolerance does not seem to diminish or weaken with a habitual consumption of caffeinated coffee [38
]. Further studies are needed to elucidate a mechanism or mechanisms for a possible protective effect of a habitual use of caffeinated coffee as well as of decaffeinated coffee in glucose metabolism.
The insulin parameters did not change by either caffeinated or decaffeinated coffee in the present study. The changes in the insulin-related parameters generally showed a large between-subject variation, and it may have been difficult to detect a possible effect of coffee on the insulin parameters. A suggestive increase in adiponectin concentrations observed for the caffeinated coffee group is consistent with the previous observation [17
], but the increase did not differ from the change in the noncoffee group.
There was a fairly large variation in serum and salivary caffeine concentrations in the caffeinated coffee group. Caffeine is metabolized almost exclusively by CYP1A2 in the liver. Functional genetic polymorphisms are known in the CYP1A2 gene, and the between-subject variation in caffeine metabolism is well known [40
]. Thus low caffeine concentrations do not necessarily indicate poor compliance in the caffeinated coffee group.
The 16-week intervention period, use of the standard test for glucose tolerance, and saliva collection without appointment were advantages in the present studies. However, there were several limitations. We did not have direct information as to how stable the dietary intake and physical activity were during the intervention period. Statistical adjustment was made for the change in waist circumstance, but this measure alone probably did not capture the changes in physical activity and diet which would have affected glucose metabolism. The treatment was not blind to either the participants or the investigators, but this lack of blindness did not affect the laboratory measurements. Coffee was consumed without any additives in the present study, and the findings may not be applicable to coffee drinking with sugar and/or milk. Finally, we did not measure chemical compounds contained in caffeinated and decaffeinated coffee. It was previously reported that decaffeinated instant coffee contained a slightly lower amount of chlorogenic acids than caffeinated instant coffee of the same brand [17