Fröhlich J, Schollmeyer P, Gerok W
Am J Clin Nutr. 1978 Sep;31(9):1541-6. doi: 10.1093/ajcn/31.9.1541.
Hyperglycemia and impaired glucose tolerance are well known phenomena occurring in patients with renal failure. In contrast to true diabetic subjects, an elevated ratio of insulin to glucose during the glucose tolerance test is consistently observed indicating a peripheral insulin insensitivity. Among the possible reasons, a disturbance at the cellular level seems to be most likely. There is some evidence of reduced peripheral glucose utilization on the one hand and increased hepatic glucose output--probably by stimulation of gluconeogenesis--on the other. Agents that have been suggested to be involved in these alterations of carbohydrate metabolism in uremia are hormones, electrolytes, pH, and "toxic" metabolic intermediates or end-products. Of these, an increase in insulin antagonistic hormones; among them growth hormone, catecholamines, and glucagon, seems to be of most significance. Although for the individual hormones no equivocal correlation with glucose intolerance has been proved, the interaction of all of them may result in a preponderance of insulin antagonism thus leading to an apparent insulin resistance.
高血糖和糖耐量受损是肾衰竭患者中众所周知的现象。与真正的糖尿病患者相比,在葡萄糖耐量试验期间,胰岛素与葡萄糖的比率持续升高,表明外周胰岛素不敏感。在可能的原因中,细胞水平的紊乱似乎最有可能。一方面有一些证据表明外周葡萄糖利用减少,另一方面肝脏葡萄糖输出增加——可能是通过糖异生的刺激。已被认为与尿毒症中碳水化合物代谢这些改变有关的因素有激素、电解质、pH值和“有毒”代谢中间体或终产物。其中,胰岛素拮抗激素增加;其中生长激素、儿茶酚胺和胰高血糖素似乎最为重要。尽管对于个体激素而言,尚未证明与葡萄糖不耐受有明确的相关性,但它们所有的相互作用可能导致胰岛素拮抗占优势,从而导致明显的胰岛素抵抗。