Kobayashi Misato, Kurata Takao, Hamana Yoshiki, Hiramitsu Masanori, Inoue Takashi, Murai Atsushi, Horio Fumihiko
Department of Applied Molecular Bioscience, Graduate School of Bioagricultural Sciences, Nagoya University.
Research & Development Division, Pokka Sapporo Food & Beverage Ltd.
J Nutr Sci Vitaminol (Tokyo). 2017;63(3):200-207. doi: 10.3177/jnsv.63.200.
Coffee consumption reduces the risk of type 2 diabetes in humans, but the mechanism remains unclear. In this study, we investigated the effect of coffee on pancreatic β-cells in the induction of diabetes by streptozotocin (STZ) treatment in mice. We examined the effect of coffee, caffeine, or decaffeinated coffee ingestion on STZ-induced hyperglycemia. After STZ injection in Exp. 1 and 2, serum glucose concentration and water intake in coffee ingestion (Coffee group) tended to be lowered or was significantly lowered compared to those in water ingestion (Water group) instead of coffee. In Exp. 1, the values for water intake and serum glucose concentration in caffeine ingestion (Caffeine group) were similar to those in the Water group. In Exp. 2, serum glucose concentrations in the decaffeinated coffee ingestion (Decaf group) tended to be lower than those in the Water group. Pancreatic insulin contents tended to be higher in the Coffee and Decaf groups than in the Water group (Exp. 1 and 2). In Exp. 3, subsequently, we showed that coffee ingestion also suppressed the deterioration of hyperglycemia in diabetic mice which had been already injected with STZ. This study showed that coffee ingestion prevented the development of STZ-induced diabetes and suppressed hyperglycemia in STZ-diabetic mice. Caffeine or decaffeinated coffee ingestion did not significantly suppress STZ-induced hyperglycemia. These results suggest that the combination of caffeine and other components of decaffeinated coffee are needed for the preventive effect on pancreatic β-cell destruction. Coffee ingestion may contribute to the maintenance of pancreatic insulin contents.
饮用咖啡可降低人类患2型糖尿病的风险,但其机制尚不清楚。在本研究中,我们调查了咖啡对链脲佐菌素(STZ)诱导的糖尿病小鼠胰腺β细胞的影响。我们检测了饮用咖啡、咖啡因或脱咖啡因咖啡对STZ诱导的高血糖的影响。在实验1和实验2中注射STZ后,与饮用清水组(清水组)相比,饮用咖啡组(咖啡组)的血清葡萄糖浓度和饮水量趋于降低或显著降低。在实验1中,饮用咖啡因组(咖啡因组)的饮水量和血清葡萄糖浓度值与清水组相似。在实验2中,饮用脱咖啡因咖啡组(脱咖啡因咖啡组)的血清葡萄糖浓度趋于低于清水组。咖啡组和脱咖啡因咖啡组的胰腺胰岛素含量趋于高于清水组(实验1和实验2)。随后在实验3中,我们发现饮用咖啡还可抑制已注射STZ的糖尿病小鼠高血糖的恶化。本研究表明,饮用咖啡可预防STZ诱导的糖尿病的发生,并抑制STZ诱导的糖尿病小鼠的高血糖。饮用咖啡因或脱咖啡因咖啡并未显著抑制STZ诱导的高血糖。这些结果表明,咖啡因与脱咖啡因咖啡的其他成分结合才具有预防胰腺β细胞破坏的作用。饮用咖啡可能有助于维持胰腺胰岛素含量。