Conway G S, Clark P M, Wong D
Department of Medicine, University College and Middlesex Hospitals, London, UK.
Clin Endocrinol (Oxf). 1993 Feb;38(2):219-22. doi: 10.1111/j.1365-2265.1993.tb00996.x.
Hyperinsulinaemia in the polycystic ovary syndrome (PCOS) has previously been defined using polyclonal radioimmunoassays (RIA) in which partially processed insulin-like molecules cross-react. This study aimed to reassess hyperinsulinaemia in women with PCOS using specific immunoradiometric assays (IRMA) for insulin, proinsulin and 32-33 split proinsulin.
Patients attended for 75 g oral glucose tolerance tests and were divided into groups depending on their degree of obesity and fasting insulin status determined by RIA. IRMA measurements for insulin-like molecules in plasma from patients with PCOS and controls were compared.
Thirty-four patients with ultrasound diagnosed PCOS presented to a reproductive endocrinology clinic. A control group comprised women with normal ovaries on ultrasound. Four groups were constructed, two with normal fasting insulin concentrations (lean PCOS and controls) and two with hyperinsulinaemia (lean and obese PCOS).
Plasma glucose, insulin (RIA and IRMA), proinsulin and 32-33 split proinsulin concentrations were measured at time 0, 30 and 120 minutes of an oral glucose tolerance test.
Hyperinsulinaemia determined by RIA in lean and obese women with PCOS was confirmed using a specific IRMA assay for insulin. Plasma proinsulin and 32-33 split proinsulin concentrations were higher in hyperinsulinaemic women with PCOS compared with women with normal insulin concentrations. The proportion of circulating insulin-like molecules represented by proinsulin and 32-33 split proinsulin was similar in all groups studied.
Hyperinsulinaemia in PCOS is likely to reflect insulin resistance because the raised concentrations of proinsulin and 32-33 split proinsulin were in proportion to the raised insulin concentrations. Hyperinsulinaemia in PCOS, defined by RIA, therefore differs from that in non-insulin dependent diabetes mellitus where it is largely accounted for by disproportionate hyperproinsulinaemia.
多囊卵巢综合征（PCOS）中的高胰岛素血症以前是使用多克隆放射免疫测定法（RIA）来定义的，在这种方法中，部分加工的胰岛素样分子会发生交叉反应。本研究旨在使用针对胰岛素、胰岛素原和32 - 33裂解胰岛素原的特异性免疫放射测定法（IRMA）重新评估PCOS女性中的高胰岛素血症。
患者接受75克口服葡萄糖耐量试验，并根据其肥胖程度和通过RIA测定的空腹胰岛素状态进行分组。比较PCOS患者和对照组血浆中胰岛素样分子的IRMA测量值。
34名经超声诊断为PCOS的患者到生殖内分泌诊所就诊。一个对照组由超声检查卵巢正常的女性组成。构建了四组，两组空腹胰岛素浓度正常（瘦型PCOS组和对照组），两组有高胰岛素血症（瘦型和肥胖型PCOS组）。
在口服葡萄糖耐量试验的0、30和120分钟时测量血浆葡萄糖、胰岛素（RIA和IRMA法）、胰岛素原和32 - 33裂解胰岛素原浓度。
使用针对胰岛素的特异性IRMA测定法证实了瘦型和肥胖型PCOS女性中通过RIA测定的高胰岛素血症。与胰岛素浓度正常的女性相比，高胰岛素血症的PCOS女性血浆胰岛素原和32 - 33裂解胰岛素原浓度更高。在所有研究组中，胰岛素原和32 - 33裂解胰岛素原所代表的循环胰岛素样分子比例相似。
PCOS中的高胰岛素血症可能反映胰岛素抵抗，因为胰岛素原和32 - 33裂解胰岛素原浓度的升高与胰岛素浓度的升高成比例。因此，由RIA定义的PCOS中的高胰岛素血症与非胰岛素依赖型糖尿病中的高胰岛素血症不同，在非胰岛素依赖型糖尿病中，高胰岛素血症主要由不成比例的高胰岛素原血症引起。
