Sekiguchi Y, Kasai K, Hasegawa K, Suzuki Y, Shimoda S
Department of Endocrinology, Dokkyo University School of Medicine, Tochigi, Japan.
Life Sci. 1994;55(15):1219-28. doi: 10.1016/0024-3205(94)00661-x.
When pituitary adenylate cyclase activating polypeptide (PACAP-38, 420 pmol/kg) was injected to anesthetized dogs, hyperglycemia associated with elevation in plasma glucagon and adrenalin levels was observed. In dogs undergone adrenalectomy, the same dose of it stimulated insulin, but not glucagon, release and hyperglycemia was not observed. Much higher dose was needed to evoke hyperglycemia in such dogs. Next, direct glycogenolytic activities of PACAP, glucagon and adrenalin were studied on cultured rat hepatocytes. PACAP38 stimulated glucose output via cAMP production by the cells, but the potency was far less than that of glucagon. Adrenalin, however, could not exert the activity with physiological concentrations. These results indicate that hyperglycemic effect of PACAP can be attributed mainly to indirect effects resulting from glucagon and adrenalin release and possibly in part to a direct action on hepatocytes.
当向麻醉的犬注射垂体腺苷酸环化酶激活多肽（PACAP - 38，420 pmol/kg）时，观察到血糖升高，同时血浆胰高血糖素和肾上腺素水平也升高。在接受肾上腺切除术的犬中，相同剂量的该多肽刺激胰岛素释放，但不刺激胰高血糖素释放，且未观察到血糖升高。在这类犬中需要更高剂量才能诱发血糖升高。接下来，在培养的大鼠肝细胞上研究了PACAP、胰高血糖素和肾上腺素的直接糖原分解活性。PACAP38通过细胞产生cAMP刺激葡萄糖输出，但其效力远低于胰高血糖素。然而，肾上腺素在生理浓度下不能发挥这种活性。这些结果表明，PACAP的高血糖作用主要可归因于胰高血糖素和肾上腺素释放产生的间接作用，可能部分归因于对肝细胞的直接作用。
