Halter J B, Beard J C, Porte D
Am J Physiol. 1984 Jul;247(1 Pt 1):E47-52. doi: 10.1152/ajpendo.1984.247.1.E47.
Catecholamines and a number of other hormones released during stress states contribute to the development of hyperglycemia by directly stimulating glucose production and interfering with tissue disposal of glucose. However, hyperglycemia stimulates the secretion of insulin and inhibits the secretion of glucagon, effects that will diminish the degree of hyperglycemia resulting from direct actions of stress hormones on glucose production and disposal. The key additional role of catecholamines in the development of stress hyperglycemia is interference with the normal feedback control of insulin and glucagon secretion by circulating glucose levels. Although pancreatic islet responses to hyperglycemia may be modulated by catecholamines, any increase of insulin secretion or suppression of glucagon secretion that does occur may be important for limiting the degree of elevation of circulating glucose that results. Thus, plasma insulin and glucagon levels during stress states will reflect the interaction between the opposing effects of hyperglycemia and catecholamines. Diabetic patients who have impaired islet responses to glucose will be particularly prone to the development of marked hyperglycemia during stress states because they may be unable to respond to the influence of hyperglycemia in counteracting adrenergic inhibition of insulin secretion and stimulation of glucagon secretion.
在应激状态下释放的儿茶酚胺和许多其他激素，通过直接刺激葡萄糖生成并干扰葡萄糖的组织代谢，促使高血糖症的发生。然而，高血糖会刺激胰岛素分泌并抑制胰高血糖素分泌，这些作用会减轻应激激素对葡萄糖生成和代谢的直接作用所导致的高血糖程度。儿茶酚胺在应激性高血糖发生过程中的关键额外作用是干扰循环葡萄糖水平对胰岛素和胰高血糖素分泌的正常反馈控制。尽管儿茶酚胺可能会调节胰岛对高血糖的反应，但确实发生的胰岛素分泌增加或胰高血糖素分泌抑制，对于限制由此导致的循环葡萄糖升高程度可能很重要。因此，应激状态下的血浆胰岛素和胰高血糖素水平将反映高血糖和儿茶酚胺相反作用之间的相互作用。胰岛对葡萄糖反应受损的糖尿病患者，在应激状态下特别容易发生明显的高血糖，因为他们可能无法应对高血糖在抵消肾上腺素能对胰岛素分泌的抑制和对胰高血糖素分泌的刺激方面的影响。
