Locatelli V, Petraglia F, Tirloni N, Müller E E
Life Sci. 1986 Jan 27;38(4):379-86. doi: 10.1016/0024-3205(86)90086-x.
The concentrations of beta-endorphin like immunoreactivity (beta-END) in the hypothalamus, pituitary and plasma were studied in rats of either sex, one month after induction of diabetes by single iv injection of streptozotocin. As controls, both normal and undernourished rats, weight-matched with diabetic rats, were used. Diabetic male and female rats had a marked depletion of beta-END stores in the hypothalamus and neurointermediate lobe (NIL) but not in the anterior pituitary. Depletion of beta-END was reversed to normal by insulin replacement therapy. Severe undernourishment was not as effective as diabetes to reduce beta-END stores in the hypothalamus and NIL. A significant reduction of beta-END was observed only in the NIL of undernourished female rats. Plasma beta-END and beta-lipotropin (beta-LPH) concentrations were not significantly altered in diabetic rats. These results indicate that the lack of insulin may affect beta-END synthesis in the hypothalamus and NIL.
通过单次静脉注射链脲佐菌素诱导糖尿病一个月后，对雌雄大鼠下丘脑、垂体和血浆中β-内啡肽样免疫反应性（β-END）的浓度进行了研究。作为对照，使用了体重与糖尿病大鼠匹配的正常和营养不良大鼠。糖尿病雄性和雌性大鼠下丘脑和神经中间叶（NIL）中的β-END储备明显减少，但垂体前叶未减少。胰岛素替代疗法可将β-END的消耗逆转至正常。严重营养不良在减少下丘脑和NIL中β-END储备方面不如糖尿病有效。仅在营养不良雌性大鼠的NIL中观察到β-END显著降低。糖尿病大鼠血浆β-END和β-促脂素（β-LPH）浓度无显著变化。这些结果表明，胰岛素缺乏可能影响下丘脑和NIL中β-END的合成。
