Turner R C, Hart G, London D R
Diabetologia. 1977 Jan;13(1):19-23. doi: 10.1007/BF00996322.
Basal insulin secretion has been thought to be via a different mechanism from stimulated insulin secretion, partly because it is not similarly suppressed by adrenalin. However, adrenalin normally causes hyperglycaemia, but if it is infused while the plasma glucose is kept constant there is marked suppression of insulin secretion. Sympathetic stimulation modulates basal insulin secretion, and alpha adrenergic blockade impaired the suppression of insulin secretion in response to hypoglycaemia. Four of five benign insulinomas had marked suppression of insulin secretion by adrenalin, but one malignant and one benign insulionoma had little suppression. Both had a raised proportion of their basal plasma insulin as proinsulin, and the impaired suppression of secretion by adrenalin probably signified an undifferentiated tumour.
基础胰岛素分泌一直被认为其机制与刺激后的胰岛素分泌不同,部分原因是它不会被肾上腺素类似地抑制。然而,肾上腺素通常会导致血糖升高,但如果在血浆葡萄糖保持恒定的情况下输注肾上腺素,胰岛素分泌会受到显著抑制。交感神经刺激调节基础胰岛素分泌,α肾上腺素能阻断会削弱对低血糖反应时胰岛素分泌的抑制作用。五分之四的良性胰岛素瘤对肾上腺素刺激的胰岛素分泌有显著抑制,但有一例恶性胰岛素瘤和一例良性胰岛素瘤几乎没有受到抑制。两者基础血浆胰岛素中胰岛素原的比例均升高,肾上腺素对分泌抑制作用的受损可能表明肿瘤未分化。