Sener A, Malaisse W J
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Arch Biochem Biophys. 1988 Feb 15;261(1):16-26. doi: 10.1016/0003-9861(88)90099-9.
D-Fructose (3.3 to 33.0 mmol/liter) caused a concentration-related increase in insulin output from rat islets exposed to D-glucose (3.3 to 7.0 mmol/liter), such an increase not being more marked in mouse islets. The fructose-induced increment in insulin release, relative to that evoked by D-glucose, was two times higher in islets exposed to D-glucose than in islets stimulated by D-mannose, 2-ketoisocaproate, or nonnutrient secretagogs. Likewise, the metabolism of D-fructose in islet cells was significantly different in the absence or presence of D-glucose. Thus, the ketose was largely channeled into the pentose phosphate pathway in glucose-deprived, but not so in glucose-stimulated, islets. In both glucose-deprived and glucose-stimulated islets, however, the magnitude of the secretory response to D-fructose was commensurate with the increase in ATP production attributable to its catabolism. These findings indicate that the metabolic fate of hexoses--and, hence, their insulinotropic capacity--is not ruled solely at the level of their phosphorylation.
D-果糖（3.3至33.0毫摩尔/升）可使暴露于D-葡萄糖（3.3至7.0毫摩尔/升）的大鼠胰岛的胰岛素分泌量呈浓度依赖性增加，而这种增加在小鼠胰岛中并不明显。相对于由D-葡萄糖引起的胰岛素释放增加，在暴露于D-葡萄糖的胰岛中，果糖诱导的胰岛素释放增加量比由D-甘露糖、2-酮异己酸或非营养性促分泌剂刺激的胰岛中高两倍。同样，在有无D-葡萄糖的情况下，胰岛细胞中D-果糖的代谢也存在显著差异。因此，在葡萄糖缺乏的胰岛中，酮糖主要进入磷酸戊糖途径，但在葡萄糖刺激的胰岛中并非如此。然而，在葡萄糖缺乏和葡萄糖刺激的胰岛中，对D-果糖的分泌反应强度均与因其分解代谢导致的ATP生成增加量相当。这些发现表明，己糖的代谢命运——以及因此它们的促胰岛素分泌能力——并非仅由其磷酸化水平决定。
