Le Feuvre R A, Woods A J, Stock M J, Rothwell N J
Department of Physiological Sciences, University of Manchester, U.K.
Brain Res. 1991 Apr 26;547(1):110-4.
Intra-cerebroventricular (i.c.v.) injection of glucose (0.1-1.0 mumol) caused dose-dependent increases in resting oxygen consumption (Vo2) of conscious rats (maximum increase of 15.4 +/- 2% at 0.5 mumol). These effects were significantly attenuated by peripheral (i.p.) pretreatment with the beta-adrenoceptor propranolol, indicating the importance of the sympathetic nervous system (SNS) in the response. Plasma glucose concentrations were elevated (11%) 30 min after central injection of glucose, but intravenous glucose (0.5 mumol) did not affect resting Vo2. Animals which had been fasted for 12 h prior to Vo2 measurement exhibited reduced basal Vo2 values, but the nutritional state of the animal did not affect the metabolic response to central injections of glucose (0.5 mumol). Rats exhibiting genetic (fa/fa Zucker rats) and hypothalamic (VMH-lesioned) obesity showed similar thermogenic responses to centrally administered glucose, to their lean counterparts. These data suggest a dual action of central glucose in the regulation of energy balance, involving stimulation of energy expenditure in addition to its reported inhibition of energy intake. The defective diet-induced thermogenesis associated with VMH and genetic obesities does not appear to result from an inability to respond to changes in intracerebroventricular glucose concentrations.
向清醒大鼠脑室内(i.c.v.)注射葡萄糖(0.1 - 1.0微摩尔)会导致静息耗氧量(Vo2)呈剂量依赖性增加(0.5微摩尔时最大增加15.4 +/- 2%)。外周(i.p.)预先用β - 肾上腺素能受体拮抗剂普萘洛尔处理可显著减弱这些效应,表明交感神经系统(SNS)在该反应中起重要作用。脑室内注射葡萄糖30分钟后血浆葡萄糖浓度升高(11%),但静脉注射葡萄糖(0.5微摩尔)不影响静息Vo2。在进行Vo2测量前禁食12小时的动物基础Vo2值降低,但动物的营养状态不影响对脑室内注射葡萄糖(0.5微摩尔)的代谢反应。表现出遗传性(fa/fa Zucker大鼠)和下丘脑性(VMH损伤)肥胖的大鼠对脑室内给予葡萄糖的产热反应与其瘦型对应物相似。这些数据表明中枢葡萄糖在能量平衡调节中具有双重作用,除了其已报道的抑制能量摄入外,还涉及刺激能量消耗。与VMH和遗传性肥胖相关的饮食诱导性产热缺陷似乎并非源于对脑室内葡萄糖浓度变化无反应的能力。