DiRocco R J, Grill H J
Science. 1979 Jun 8;204(4397):1112-4. doi: 10.1126/science.451558.
The reduction of glycolysis by hypoglycemia or the glucose analog 2-deoxy-D-glucose (2DG) stimulates compensatory sympathetic alterations of metabolism. Considerable attention has been focused on the hypothalamus as the probable locus of requisite metabolic signal detection. We report, however, that unanesthetized chronically decerebrate rats are capable of exhibiting sympathoadrenal hyperglycemia in response to the metabolic challenge presented by 2DG. This findings demonstrates that the forebrain is not necessary for glucoprivic stimulation of this reflex. Since cervical cord transection has been shown to eliminate hyperglycemia induced by 2DG, we conclude that the caudal brainstem contains an essential part of the neural mechanism which both detects metabolic need and ameliorates that need through the release of stored fuels.
低血糖或葡萄糖类似物2-脱氧-D-葡萄糖（2DG）导致的糖酵解减少会刺激代谢的代偿性交感神经改变。下丘脑作为必要代谢信号检测的可能位点，已受到相当多的关注。然而，我们报告称，未麻醉的慢性去大脑大鼠能够对2DG带来的代谢挑战做出交感肾上腺性高血糖反应。这一发现表明，前脑对于这种反射的糖缺乏刺激并非必需。由于已证明颈髓横断可消除2DG诱导的高血糖，我们得出结论，延髓尾部包含神经机制的一个重要部分，该部分既能检测代谢需求，又能通过释放储存的燃料来缓解这种需求。
