Ishimori M, Takeda N, Okumura S, Murai T, Inouye H, Yasuda K
Third Department of Internal Medicine, Gifu University School of Medicine, Japan.
Clin Endocrinol (Oxf). 1994 Oct;41(4):433-8. doi: 10.1111/j.1365-2265.1994.tb02573.x.
Primary aldosteronism is a recognized endocrine cause of glucose intolerance. A blunted insulin response to glucose in patients with primary aldosteronism is well known, but insulin sensitivity has not been thoroughly determined. We investigated insulin sensitivity and insulin secretion in patients with aldosterone producing adenoma.
Glucose tolerance and insulin responses to glucose were evaluated using a standard 75 g oral glucose tolerance test in patients with aldosterone producing adenoma before and after surgery, and in control subjects. Parameters for insulin resistance (HOMA-R) and pancreatic beta-cell function (HOMA-beta F) were derived from a homeostasis model assessment.
Fifteen patients with aldosterone producing adenoma and 41 control subjects with normal glucose tolerance matched for age and body mass index, were studied. Eight patients were re-evaluated after surgical removal of the adenoma. In 5 patients 125I-insulin binding to erythrocytes was also measured.
Plasma glucose was measured by a glucose oxidase method. Plasma insulin, aldosterone and renin activity were measured by radioimmunoassay.
Both fasting plasma glucose and insulin were lower in the patients than in the controls. Although the areas under the curve for plasma glucose during the oral glucose tolerance test did not differ, that for plasma insulin was less in the patients with hyperaldosteronism. Insulin sensitivity was increased in the patients, as evidenced by decreased HOMA-R compared with controls, while HOMA-beta F was comparable between the groups. 125I-insulin binding to erythrocytes was higher in 5 patients than in 19 normal controls. After surgical removal of adenoma, neither fasting plasma glucose nor the glucose area under the curve during the oral glucose tolerance test changed. However, fasting plasma insulin and the insulin area under the curve increased significantly. HOMA-R increased and HOMA-beta F remained unaltered.
Insulin sensitivity was increased in untreated patients with aldosterone producing adenoma. Enhanced insulin receptor binding may contribute to this increased insulin sensitivity.
原发性醛固酮增多症是一种公认的导致葡萄糖耐量异常的内分泌病因。原发性醛固酮增多症患者对葡萄糖的胰岛素反应减弱是众所周知的，但胰岛素敏感性尚未得到充分测定。我们研究了醛固酮瘤患者的胰岛素敏感性和胰岛素分泌情况。
采用标准的75克口服葡萄糖耐量试验，对醛固酮瘤患者手术前后及对照受试者进行葡萄糖耐量和胰岛素对葡萄糖反应的评估。胰岛素抵抗（HOMA-R）和胰腺β细胞功能（HOMA-βF）参数通过稳态模型评估得出。
研究了15例醛固酮瘤患者和41例年龄及体重指数匹配的糖耐量正常的对照受试者。8例患者在手术切除腺瘤后进行了重新评估。还对5例患者测定了125I胰岛素与红细胞的结合情况。
采用葡萄糖氧化酶法测定血浆葡萄糖。采用放射免疫分析法测定血浆胰岛素、醛固酮和肾素活性。
患者的空腹血浆葡萄糖和胰岛素均低于对照组。虽然口服葡萄糖耐量试验期间血浆葡萄糖的曲线下面积无差异，但醛固酮增多症患者的血浆胰岛素曲线下面积较小。患者的胰岛素敏感性增加，与对照组相比HOMA-R降低即证明了这一点，而两组之间的HOMA-βF相当。5例患者的125I胰岛素与红细胞的结合高于19例正常对照。手术切除腺瘤后，空腹血浆葡萄糖和口服葡萄糖耐量试验期间的曲线下葡萄糖面积均未改变。然而，空腹血浆胰岛素和曲线下胰岛素面积显著增加。HOMA-R增加，HOMA-βF保持不变。
未经治疗的醛固酮瘤患者胰岛素敏感性增加。胰岛素受体结合增强可能导致这种胰岛素敏感性增加。
