King B M, Stamoutsos B A, Grossman S P
Pharmacol Biochem Behav. 1978 Mar;8(3):259-62. doi: 10.1016/0091-3057(78)90313-1.
A dose-response relationship for the effects of 2-deoxy-D-glucose (2-DG) (0-400 mg/kg) on food intake was established in normal and obese ventromedial hypothalamic lesioned rats. In normal animals the lowest dose that produced a statistically signififant increase over baseline food intake was 100 mg/kg 2-DG. Larger doses produced a progressively greater effect. Most of the increase in food intake occurred during the first hour after the injection of 2-DG, the latency of the first feeding bout being shorter for higher doses of the compound. Obese VMH rats significantly increased their 4-hr food intake after 150, 200, and 250, and 400 mg/kg 2-DG, but the increase in feeding was delayed compared to control animals. During the first hour after the injection, the food intake of obese rats was unaffected by doses of 2-DG up to 250 mg/kg, and inhibited by higher doses (300 and 400 mg/kg). The effects of VMH lesions on 2-DG-induced eating are attributed to the elimination of afferents from peripheral glucoreceptors.
在正常和肥胖的腹内侧下丘脑损伤大鼠中，建立了2-脱氧-D-葡萄糖（2-DG）（0-400毫克/千克）对食物摄入量影响的剂量反应关系。在正常动物中，与基线食物摄入量相比产生统计学显著增加的最低剂量是100毫克/千克2-DG。更高剂量产生的效果逐渐增强。食物摄入量的增加大多发生在注射2-DG后的第一小时内，化合物剂量越高，首次进食发作的潜伏期越短。肥胖的腹内侧下丘脑损伤大鼠在注射150、200、250和400毫克/千克2-DG后，4小时食物摄入量显著增加，但与对照动物相比，进食增加出现延迟。在注射后的第一小时内，高达250毫克/千克剂量的2-DG对肥胖大鼠的食物摄入量没有影响，而更高剂量（300和400毫克/千克）则会抑制食物摄入。腹内侧下丘脑损伤对2-DG诱导进食的影响归因于外周葡萄糖感受器传入神经的消除。
