Shiraishi Jun-Ichi, Yanagita Kouchi, Fujita Masanori, Bungo Takashi
Laboratory of Animal Behavior and Physiology, Graduate School of Biosphere Science, Hiroshima University, 1-4-4 Kagamiyama, Higashi-Hiroshima 739-8528, Japan.
Neurosci Lett. 2008 Jul 18;439(3):227-9. doi: 10.1016/j.neulet.2008.05.040. Epub 2008 May 16.
Pro-opiomelanocortin (POMC) neurons in the hypothalamus are direct targets of peripheral satiety signals, such as leptin and insulin in mammals. The stimulation of these signals activates hypothalamic POMC neurons and elevates POMC-derived melanocortin peptides that inhibit food intake in mammals. On the other hand, it has been recognized that beta-endorphin, a post-translational processing of POMC, acts in an autoreceptor manner to the micro-opioid receptor (MOR) on POMC neurons, diminishing POMC neuronal activity in mammals. Recently, we found that central insulin functions as an anorexic peptide in chicks. Thus, the present study was done to elucidate whether beta-endorphin affects the activation of POMC neurons by insulin in neonatal chicks. Consequently, quantitative real-time PCR analysis shows that intracerebroventricular (ICV) injection of insulin with beta-endorphin significantly decreases brain POMC mRNA expression when compared with insulin alone. In addition, co-injection of MOR agonist (beta-endorphin or [d-Ala2, N-MePhe4, Gly5-ol]-enkephalin (DAMGO)) significantly attenuates insulin-induced hypophagia in chicks. These data suggest that beta-endorphin regulates the activity of the central melanocortin system, and its activation may provide an inhibitory feedback mechanism in the brain of neonatal chicks.
下丘脑的阿片-促黑素原（POMC）神经元是外周饱腹感信号的直接靶点，如哺乳动物体内的瘦素和胰岛素。这些信号的刺激会激活下丘脑POMC神经元，并提高源自POMC的促黑素肽水平，从而抑制哺乳动物的食物摄入。另一方面，人们已经认识到，β-内啡肽作为POMC的一种翻译后加工产物，以自受体的方式作用于POMC神经元上的微阿片受体（MOR），降低哺乳动物POMC神经元的活性。最近，我们发现中枢胰岛素在雏鸡中作为一种厌食肽发挥作用。因此，本研究旨在阐明β-内啡肽是否会影响新生雏鸡中胰岛素对POMC神经元的激活作用。结果，定量实时PCR分析表明，与单独注射胰岛素相比，脑室内（ICV）注射胰岛素和β-内啡肽会显著降低脑中POMC mRNA的表达。此外，共同注射MOR激动剂（β-内啡肽或[D-Ala2，N-MePhe4，Gly5-ol]-脑啡肽（DAMGO））会显著减弱雏鸡中胰岛素诱导的摄食减少。这些数据表明，β-内啡肽调节中枢促黑素系统的活性，其激活可能在新生雏鸡的大脑中提供一种抑制性反馈机制。
