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Coffee intake, glucose metabolism and gene polymorphisms

Published online by Cambridge University Press:  23 July 2018

Tomoyuki Kawada*
Affiliation:
Department of Hygiene and Public Health, Nippon Medical School, Tokyo 113-8602, Japan
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Abstract

Type
Letter to the Editor
Copyright
© The Authors 2018 

Robertson et al. ( Reference Robertson, Clifford and Penson 1 ) conducted a randomised study to investigate the effects of regular coffee intake on markers of glucose and lipid metabolism with special reference to rs762551 SNP in the CYP1A2 gene. Before coffee intake, the AC genotype subjects with slow caffeine metabolism presented higher baseline glucose and NEFA than the AA genotype subjects with fast caffeine metabolism. Post-intervention, reduced postprandial glycaemia and NEFA were observed in the AC genotype subjects, which significantly differed from the change in the AA genotype subjects. The authors were cautious with regard to one-size-fits-all recommendation for coffee drinking and development of type 2 diabetes (T2D), because genotype and intervention were closely related to the association. I have a concern about their study related to type 2 diabetes mellitus (T2DM).

Denden et al.( Reference Denden, Bouden and Haj Khelil 2 ) conducted a meta-analysis to clarify the association between the CYP1A2 rs762551 polymorphism and habitual coffee intake with particular reference to sex and ethnicity. OR of genotypes AA against AC+CC for coffee intake was 1·13 (95 % CI 1·03, 1·24). In subgroup analyses, OR of genotypes AA against AC+CC in male, younger and Caucasian subjects for coffee intake were 1·21 (95 % CI 1·08, 1·35), 1·71 (95 % CI 1·18, 2·48) and 1·29 (95 % CI 1·12, 1·49), respectively. They concluded that the rs762551 AA genotype was closely associated with higher coffee intake, especially in the three presented subgroups. I suppose that the advantage of the AA genotype subjects for rapid caffeine metabolism would be lead to diminish the suppression of insulin sensitivity by habitual coffee intake, which would be supported by the preventive effect of decaffeinated coffee on incident T2DM( Reference Huxley, Lee and Barzi 3 ). Glucose-lowering effect by chlorogenic acids is explained by the suppression of hepatic glucose-6-phosphate activity( Reference Herling, Burger and Schwab 4 ), and the reduced risk of developing T2DM by regular coffees would be explained by the combination of chlorogenic acids and caffeine intake( Reference Santos and Lima 5 ).

Robertson et al. also pointed out the interventional effect in the AC genotype subjects of the postprandial glycaemic and lipaemic responses to chronic coffee consumption. Mechanisms of interventional effect on both glucose and NEFA should be specified by further study.

Acknowledgements

This research received no specific grant from any funding agency, commercial or not-for-profit sectors.

The author declares that there are no conflicts of interest.

References

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