肿瘤患者糖耐量受损的机制。
Mechanism of impaired glucose tolerance in patients with neoplasia.
作者信息
Jasani B, Donaldson L J, Ratcliffe J G, Sokhi G S
出版信息
Br J Cancer. 1978 Aug;38(2):287-92. doi: 10.1038/bjc.1978.200.
Abstract
The disappearance rate (k) of i.v. glucose was measured in cachectic and non-cachectic cancer patients and tumour-free controls. The respective k values were found to be 1.06 +/- 0.27 (mean +/- s.d.), 1.64 +/- 0.34 and 1.63 +/- 0.23. Of the other parameters measured, only plasma albumin level was found to vary significantly amongst the 3 categories, the mean level being the lowest in cachectic cancer patients. The means of total plasma protein, fasting blood glucose and plasma liver enzyme concentrations were similar in the 3 groups. Glucagon, a potent insulin secretogogue, failed to augment the fasting insulin level in cachectic but did so in non-cachectic cancer patients. Taken together, the findings suggest that the reduced glucose tolerance in patients with neoplasia is due to impairment of insulin release exhibited predominantly by ill-nourished advanced cancer patients having a moderate to sever degree of hypoalbuminemia.
摘要
在恶病质和非恶病质癌症患者以及无肿瘤对照中测量了静脉注射葡萄糖的消失率（k）。发现各自的k值分别为1.06±0.27（平均值±标准差）、1.64±0.34和1.63±0.23。在测量的其他参数中，仅发现血浆白蛋白水平在这三类中存在显著差异，恶病质癌症患者的平均水平最低。三组的总血浆蛋白、空腹血糖和血浆肝酶浓度平均值相似。胰高血糖素是一种有效的胰岛素分泌刺激剂，未能提高恶病质患者的空腹胰岛素水平，但在非恶病质癌症患者中可以提高。综合来看，这些发现表明肿瘤患者葡萄糖耐量降低是由于胰岛素释放受损，这主要表现为患有中度至重度低白蛋白血症的营养不良晚期癌症患者。
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