Sweeney E A, Juan C S, AvRuskin T W
Am J Med Sci. 1979 Mar-Apr;277(2):153-62. doi: 10.1097/00000441-197903000-00003.
Ten children with XO gonadal dysgenesis and ten control siblings (CS) had sequential IV tolbutamide and IM glucagon tests to ascertain serum and salivary insulin concentrations, to confirm the presence of parotid salivary insulin and to determine if these concentrations were of diagnostic value in the diagnosis of insulin deficiency. After tolbutamide, peak serum insulin concentrations were lower in the patients with Turner's syndrome (TS) than in control siblings (58 +/- 10 vs 90 +/- 15 microU/ml) and fractional areas under insulin curves were significantly lower in the patients with Turner's syndrome at 10 to 15 minutes (TS: 240 +/- 16 microUmin/ml; CS: 340 +/- 46 microU-min/ml, P less than 0.05) and at 15 to 30 minutes (TS: 562 +/- 62 microU-min/ml; CS: 884 +/- 128 microU-min/ml, P less than 0.05). After glucagon, peak serum insulin concentrations were significantly lower in Turner's syndrome than in control siblings(P less than 0.02, at 45 minutes) and fractional areas under insulin curves were also lower in TS than in siblings at 30 to 45 minutes (TS: 1,062 +/- 185 microU-min/ml; CS: 2,189 +/- 402 microU-min/ml, P less than 0.02). Basal salivary immunoreactive insulin (IR) concentrations were similar in both groups: TS: 4.8 +/- 2.1 microU/min; CS: 2.1 +/- 0.4 microU/min. Peak salivary IRI concentrations after tolbutamide were 13.8 +/- 4.7 microU/min in Turner's syndrome and 8.8 +/- 1.8 microU/ml in control siblings. Peak salivary IRI values in Turner's syndrome and in control siblings after glucagon were 26.8 +/- 10.1 and 13.4 +/- 2.1 microU/min, respectively. While significant differces in insulin secretion in serum were detected in the two patient groups, no differences were noted between groups when salivary insulin concentrations were compared. These data confirm serum insulin deficiency in gonadal dysgenesis, the presence of immunoreactive insulin in parotid saliva, and suggest the possibility that extrapancreatic insulin synthesis could occur in the parotid gland.
对10名患有XO性腺发育不全的儿童和10名对照同胞（CS）进行了静脉注射甲苯磺丁脲和肌肉注射胰高血糖素的序贯试验，以确定血清和唾液中的胰岛素浓度，确认腮腺唾液胰岛素的存在，并确定这些浓度在胰岛素缺乏诊断中是否具有诊断价值。注射甲苯磺丁脲后，特纳综合征（TS）患者的血清胰岛素峰值浓度低于对照同胞（分别为58±10与90±15微单位/毫升），并且在10至15分钟时，特纳综合征患者胰岛素曲线下的积分面积显著更低（TS：240±16微单位·分钟/毫升；CS：340±46微单位·分钟/毫升，P<0.05），在15至30分钟时也是如此（TS：562±62微单位·分钟/毫升；CS：884±128微单位·分钟/毫升，P<0.05）。注射胰高血糖素后，特纳综合征患者的血清胰岛素峰值浓度显著低于对照同胞（45分钟时P<0.02），并且在30至45分钟时，特纳综合征患者胰岛素曲线下的积分面积也低于同胞（TS：1,062±185微单位·分钟/毫升；CS：2,189±402微单位·分钟/毫升，P<0.02）。两组的基础唾液免疫反应性胰岛素（IR）浓度相似：TS组为4.8±2.1微单位/分钟；CS组为2.1±0.4微单位/分钟。注射甲苯磺丁脲后，特纳综合征患者的唾液IRI峰值浓度为13.8±4.7微单位/分钟，对照同胞为8.8±1.8微单位/毫升。注射胰高血糖素后，特纳综合征患者和对照同胞的唾液IRI峰值分别为26.8±10.1和13.4±2.1微单位/分钟。虽然在两组患者中检测到血清胰岛素分泌存在显著差异，但比较唾液胰岛素浓度时，两组之间未发现差异。这些数据证实了性腺发育不全患者存在血清胰岛素缺乏，腮腺唾液中存在免疫反应性胰岛素，并提示胰腺外胰岛素合成可能发生在腮腺中的可能性。
