Kahn S E, Verchere C B, D'Alessio D A, Cook D L, Fujimoto W Y
Department of Medicine, University of Washington, Seattle.
Diabetologia. 1993 Jun;36(6):570-3. doi: 10.1007/BF02743276.
To determine the potential for differential release of islet amyloid polypeptide and insulin, we performed studies in rat islet monolayer cultures under conditions known to impair regulated beta-cell secretion. In inhibiting concentrations of epinephrine or the absence of calcium, islet amyloid polypeptide was secreted through a constitutive pathway while insulin was not. These findings suggest a mechanism for persistent islet amyloid polypeptide secretion and amyloid accumulation when regulated insulin release is impaired as in Type 2 (non-insulin-dependent) diabetes mellitus and insulinomas.
为了确定胰岛淀粉样多肽和胰岛素的差异释放潜力,我们在已知会损害β细胞调节性分泌的条件下,对大鼠胰岛单层培养物进行了研究。在肾上腺素抑制浓度下或无钙条件下,胰岛淀粉样多肽通过组成性途径分泌,而胰岛素则不分泌。这些发现提示了一种机制,即在2型(非胰岛素依赖型)糖尿病和胰岛素瘤中,当调节性胰岛素释放受损时,胰岛淀粉样多肽持续分泌及淀粉样物质积累的机制。