Angell C A, Tubbs R C, Moore A B, Barb C R, Cox N M
Department of Animal and Dairy Sciences Mississippi State University, MS 39762, USA.
Domest Anim Endocrinol. 1996 Sep;13(5):453-63. doi: 10.1016/0739-7240(96)00076-8.
The influence of the acute withdrawal of insulin therapy in streptozocin-diabetic female swine was examined for changes in 1) the in vivo pulsatile secretion of luteinizing hormone (LH), 2) the preovulatory-like gonadotropin patterns after exogenous estradiol, and 3) the in vitro LH secretion by cultured pituitary cells. In Experiment 1, ovariectomized diabetic pigs (n = 4) were maintained with insulin therapy until 4 d before estradiol benzoate (EB; 7 micrograms/kg body weight; subcutaneous) was administered. Four normal ovariectomized pigs, matched for age and weight, served as controls. The diabetic state was confirmed by the measurement of glucose and insulin concentrations during a glucose tolerance test. Pulsatile LH secretion was not influenced by experimental diabetes mellitus. However, the expected surge in LH was not induced by EB in diabetic gilts. In contrast, three of four normal gilts had a preovulatory-type surge in LH. Concentrations of follicle-stimulating hormone in serum were not affected by diabetes mellitus. Estradiol concentrations in serum after ER were influenced by diabetes mellitus (treatment by time interaction; P < 0.001). In individual estradiol profiles, maximum concentrations were similar (104 +/- 10.4 and 91 +/- 12.0 ng/ml for normal and diabetic pigs, respectively), but the interval to maximum concentration was delayed in diabetic pigs (27.5 vs. 9.0 h; SE = 3.0; P < 0.05). However, the duration of standing estrus (2.2 +/- .3 d) and the interval from EB to estrus (3.6 +/- 0.3 d) were not influenced by diabetes mellitus. In Experiment 2, LH secretion by cultured cells and residual cellular LH content were greater in the pituitaries of normal than diabetic pigs (P < 0.05), and only cells from normal pigs responded to gonadotropin-releasing hormone (GnRH), with increased production of LH (P < 0.05). In conclusion, diabetes mellitus did not affect pulsatile LH secretion but did lower the ability of exogenous estradiol to stimulate a surge in vivo and of GnRH to increase LH in vitro, suggesting that the pituitary response to estradiol and GnRH is more severely affected by diabetes than is the GnRH pulse generator.
研究了链脲佐菌素诱导糖尿病的雌性猪急性停用胰岛素治疗后，以下方面的变化：1）促黄体生成素（LH）的体内脉冲式分泌；2）外源性雌二醇后类似排卵前的促性腺激素模式；3）培养的垂体细胞的体外LH分泌。在实验1中，切除卵巢的糖尿病猪（n = 4）接受胰岛素治疗，直至给予苯甲酸雌二醇（EB；7微克/千克体重；皮下注射）前4天。4只年龄和体重匹配的正常切除卵巢的猪作为对照。通过葡萄糖耐量试验期间测量葡萄糖和胰岛素浓度来确认糖尿病状态。实验性糖尿病未影响LH的脉冲式分泌。然而，糖尿病后备母猪中EB并未诱导预期的LH激增。相比之下，4只正常后备母猪中有3只出现了排卵前类型的LH激增。血清中促卵泡激素的浓度不受糖尿病的影响。给予EB后血清中雌二醇浓度受糖尿病影响（治疗与时间交互作用；P < 0.001）。在个体雌二醇谱中，最大浓度相似（正常猪和糖尿病猪分别为104±10.4和91±12.0纳克/毫升），但糖尿病猪达到最大浓度的间隔延迟（27.5对9.0小时；标准误 = 3.0；P < 0.05）。然而，站立发情的持续时间（2.2±0.3天）以及从EB到发情的间隔（3.6±0.3天）不受糖尿病的影响。在实验2中，正常猪垂体中培养细胞的LH分泌和细胞内残余LH含量高于糖尿病猪（P < 0.05）只有正常猪的细胞对促性腺激素释放激素（GnRH）有反应，LH分泌增加（P < 0.05）。总之，糖尿病不影响LH的脉冲式分泌，但确实降低了外源性雌二醇在体内刺激激增以及GnRH在体外增加LH的能力，这表明垂体对雌二醇和GnRH的反应比GnRH脉冲发生器受糖尿病的影响更严重。
