Ionescu E, Rohner-Jeanrenaud F, Proietto J, Rivest R W, Jeanrenaud B
Laboratoires de Recherches Métaboliques, Faculty of Medicine, University of Geneva, Switzerland.
Diabetes. 1988 Jun;37(6):773-9. doi: 10.2337/diab.37.6.773.
Cephalic-phase insulin release (CPIR) and the changes in glucose turnover induced by saccharin ingestion were studied in freely moving lean and genetically obese fa/fa rats equipped with chronic catheters for blood sampling. Six-hour-fasted lean and obese rats were trained to drink 1 ml sodium saccharin (0.15%) or 1 ml glucose (70%), and blood samples were taken before and after the stimuli. As early as 1-1.5 min poststimulus, there was a significant increase in CPIR in lean and obese rats. The amplitude of the CPIR induced either by saccharin or by glucose in the obese rats was significantly higher than it was in the lean rats. The effect of saccharin ingestion on the hepatic glucose production (HGP) and the rate of glucose disappearance (Rd) was studied in 6-h-fasted lean and obese rats, under non-steady-state conditions, according to a method previously validated. Saccharin ingestion produced a significant increase in HGP and Rd in lean and obese rats compared with basal values. The saccharin-induced increments in HGP and Rd were higher in the obese than in the lean animals. We conclude that saccharin (through taste) appears to elicit parasympathetic (insulin release) and sympathetic (HGP increase) reflexes in lean and obese rats. These taste-induced changes in plasma insulin and glucose turnover are exaggerated in the obese rats and may participate in obesity and in insulin resistance of the overall syndrome.
在自由活动的瘦型和遗传性肥胖fa/fa大鼠中,研究了头期胰岛素释放(CPIR)以及糖精摄入引起的葡萄糖代谢变化,这些大鼠均配有用于采血的慢性导管。对禁食6小时的瘦型和肥胖大鼠进行训练,使其饮用1毫升糖精钠(0.15%)或1毫升葡萄糖(70%),并在刺激前后采集血样。早在刺激后1 - 1.5分钟,瘦型和肥胖大鼠的CPIR就显著增加。肥胖大鼠中由糖精或葡萄糖诱导的CPIR幅度显著高于瘦型大鼠。根据先前验证的方法,在非稳态条件下,研究了禁食6小时的瘦型和肥胖大鼠中糖精摄入对肝脏葡萄糖生成(HGP)和葡萄糖消失率(Rd)的影响。与基础值相比,糖精摄入使瘦型和肥胖大鼠的HGP和Rd显著增加。肥胖大鼠中糖精诱导的HGP和Rd增量高于瘦型动物。我们得出结论,糖精(通过味觉)似乎在瘦型和肥胖大鼠中引发副交感神经(胰岛素释放)和交感神经(HGP增加)反射。这些味觉诱导的血浆胰岛素和葡萄糖代谢变化在肥胖大鼠中被放大,可能参与了肥胖及整个综合征的胰岛素抵抗。