Terada K, Sakata T, Oomura Y, Fujimoto K, Arase K, Osanai T, Nagai Y
Physiol Behav. 1986;38(6):861-9. doi: 10.1016/0031-9384(86)90055-7.
Hypophagia induced by 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA), an endogenous short-chain polyhydroxymonocarboxylic acid, was investigated in rats. Intraperitoneal injection of 2500 mumol 2-DTA did not suppress feeding, but 2.5 mumol 2-DTA injected into the third cerebroventricle did. To efficiently transport exogenous 2-DTA into the brain, its encapsulation and delivery in specially made sulfatide liposomes was attempted. Feeding was suppressed dose-dependently by intraperitoneally injected 2-DTA in liposomes. Injection of 2500 mumol 2-DTA into the common carotid artery also suppressed feeding. Administration by either route prolonged postprandial intermeal interval with no change in meal size, as was observed after central administration of 2-DTA. Injection of 2.5 mumol 2-DTA into the third cerebroventricle elevated plasma glucose level, leaving insulin and free fatty acids unaffected. These findings, together with previous results, indicate that at least one site for the physiological action of 2-DTA is in the hypothalamic centers for food intake.
对一种内源性短链多羟基单羧酸——3,4-二羟基丁酸（2-脱氧四羟基丁酸，2-DTA）诱导大鼠食欲减退的情况进行了研究。腹腔注射2500 μmol 2-DTA并未抑制进食，但向第三脑室注射2.5 μmol 2-DTA则有此效果。为了将外源性2-DTA有效转运至脑内，尝试将其包裹于特制的硫脂脂质体中并进行递送。腹腔注射脂质体包裹的2-DTA可剂量依赖性地抑制进食。向颈总动脉注射2500 μmol 2-DTA也会抑制进食。与经中枢给予2-DTA后观察到的情况一样，通过这两种途径给药均会延长餐后餐间间隔，且餐量无变化。向第三脑室注射2.5 μmol 2-DTA会使血糖水平升高，而胰岛素和游离脂肪酸水平不受影响。这些发现与之前的结果共同表明，2-DTA生理作用的至少一个位点位于下丘脑摄食中枢。
