Singer L K, Ritter S
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman 99164-6520s, USA.
Physiol Behav. 1996 Apr-May;59(4-5):921-3. doi: 10.1016/0031-9384(95)02144-2.
Previous results have shown that IV infusion of glucose reduces feeding induced by systemic administration of 2-deoxy-D-glucose (2-DG) or 2-mercaptoacetate (MA) in rats. Because glucose is a metabolic substrate for both central and peripheral tissues, the suppression of feeding by glucose could result from either a central or peripheral metabolic effect. In the present experiment we attempted to clarify the mechanism of glucose-induced suppression of feeding induced by 2-DG and MA by administering glucose centrally during systemic metabolic challenge. Administration of glucose into the lateral ventricle was begun immediately after systemic injection of 2-DG or MA and continued intermittently during the 2-h feeding test. We found that central glucose administration significantly reduced 2-DG- but not MA-induced feeding. These results suggest that the central effects of glucose are sufficient to suppress feeding induced by systemic 2-DG and support the hypothesis that receptors responsible for 2-DG-induced feeding are located in the brain.
先前的研究结果表明，静脉输注葡萄糖可减少大鼠因全身注射2-脱氧-D-葡萄糖（2-DG）或2-巯基乙酸（MA）所诱导的进食。由于葡萄糖是中枢和外周组织的代谢底物，葡萄糖对进食的抑制作用可能源于中枢或外周的代谢效应。在本实验中，我们试图通过在全身代谢挑战期间向中枢给予葡萄糖，来阐明葡萄糖诱导的对2-DG和MA所诱导进食的抑制机制。在全身注射2-DG或MA后，立即开始向侧脑室注射葡萄糖，并在2小时的进食测试期间间歇性地持续注射。我们发现，向中枢给予葡萄糖可显著减少2-DG诱导的进食，但对MA诱导的进食没有影响。这些结果表明，葡萄糖的中枢效应足以抑制全身注射2-DG所诱导的进食，并支持负责2-DG诱导进食的受体位于大脑中的假说。
