Renauld A, von Lawzewitsch I, Pérez R L, Sverdlik R, Agüero A, Foglia V G, Rodríguez R R
Acta Diabetol Lat. 1983 Jan-Mar;20(1):47-56. doi: 10.1007/BF02629129.
We analyzed the changes in blood sugar (BS), serum immunoreactive insulin (IRI), circulating free fatty acids (FFA) and pancreatic cytology caused by estrogenization at low pharmacological dosage in female dogs. Vehicle-injected and untreated controls (anestrus) were studied as well. Neither mean basal BS nor basal serum IRI was modified by the treatments, while the mean basal serum FFA value was raised. Glucose tolerance was not modified by the estrogens while glucose y-mean was significantly raised. Hyperglycemia was higher for a longer time in estrogenized animals compared to both controls, while the profiles of hyperinsulinemia coincided. In the estrogen-treated bitches, the pancreatic B-cells contained scarse brown-stained granules near their vascular pole, as shown by an immunochemical method. In the peripheral part of the pancreas, near the acini, some solitary, poorly beta-granulated B-cells were present. During the IVGTT, serum FFA reached lower values for a longer time in the estrogenized bitches as compared to those found in both control groups. Insulin-induced hypoglycemia in the estrogenized animals coincided with the one evoked in the vehicle controls; in the semilog relationship of serum IRI and time, y-mean was lower than that observed in oil-injected controls, and insulin space was larger. The serum FFA levels of these estrogenized bitches, very high in the basal conditions, did not respond to insulin administration, and were above those found in untreated controls and also in vehicle-injected controls just at the beginning of the test. These results are discussed. We came to the conclusion that estrogenization causes some glucose intolerance in bitches while insulin sensitivity remains normal in the IVITT as studied measuring BS. The glucose intolerance is thought to be related to a reduction in glucose space and occurs despite the normality of the serum IRI response. The pancreas must have an intense secretory response in vivo as as to maintain normal IRI activity despite degranulation of the islets of Langerhans and poor islet hypertrophy and neoformation. The serum FFA changes are thought to contribute towards the tendency to adiposity in these animals.
我们分析了低药理剂量雌激素化对雌性犬血糖（BS）、血清免疫反应性胰岛素（IRI）、循环游离脂肪酸（FFA）及胰腺细胞学的影响。同时研究了注射赋形剂和未处理的对照组（处于乏情期）。各处理组均未改变平均基础血糖及基础血清IRI水平，但平均基础血清FFA值升高。雌激素未改变葡萄糖耐量，但葡萄糖y均值显著升高。与两个对照组相比，雌激素化动物的高血糖持续时间更长、程度更高，而高胰岛素血症曲线则一致。免疫化学方法显示，雌激素处理的母犬胰腺B细胞在血管极附近含有稀少的棕色染色颗粒。在胰腺外周靠近腺泡处，存在一些单个的、β颗粒较少的B细胞。在静脉葡萄糖耐量试验（IVGTT）期间，与两个对照组相比，雌激素化母犬血清FFA在更长时间内维持较低水平。雌激素化动物中胰岛素诱导的低血糖与注射赋形剂对照组的情况一致；在血清IRI与时间的半对数关系中，y均值低于注射油剂对照组，且胰岛素空间更大。这些雌激素化母犬的血清FFA水平在基础状态下非常高，对胰岛素给药无反应，且在试验开始时高于未处理对照组及注射赋形剂对照组。对这些结果进行了讨论。我们得出结论，雌激素化会导致母犬出现一定程度的葡萄糖不耐受，而在通过测量血糖进行的IVITT研究中，胰岛素敏感性保持正常。葡萄糖不耐受被认为与葡萄糖空间减少有关，尽管血清IRI反应正常，但仍会发生。胰腺在体内必须有强烈的分泌反应，以维持正常的IRI活性，尽管胰岛出现脱颗粒、胰岛肥大和新生不良。血清FFA变化被认为促成了这些动物的肥胖倾向。
