Teixeira V L, Antunes-Rodrigues J, Migliorini R H
J Lipid Res. 1973 Nov;14(6):672-7.
The blood sugar and plasma free fatty acid responses to administration of 2-deoxyglucose were determined in normal rats and in rats subjected to adrenodemedullation and/or hypothalamic deafferentation, as well as in rats with bilateral hypothalamic lesions. Adrenodemedullation of both intact and deafferentated rats reduced the 2-deoxyglucose-induced increase of blood sugar but did not affect the plasma free fatty acid response to 2-deoxyglucose in normal rats. The increases in blood sugar levels induced by the drug in intact rats were not significantly affected by deafferentation, but, in marked contrast, plasma free fatty acid mobilization after 2-deoxyglucose administration was completely suppressed in deafferentated rats, both in the presence and in the absence of the adrenal medulla. These results confirm previous observations indicating that the sympathetic nervous system and adrenalin release from the adrenal medulla participate in the production of hyperglycemia by 2-deoxyglucose. They provide, in addition, evidence for the existence, in the anterior hypothalamus or in limbic structures, of centers that can specifically influence mobilization of free fatty acids through a direct activation of the sympathetic fibers of adipose tissue without intervening in glucose homeostasis. The experiments in animals with bilateral hypothalamic lesions, although small in number, seem to support the above conclusions.
在正常大鼠、接受肾上腺髓质切除和/或下丘脑去传入神经支配的大鼠以及双侧下丘脑损伤的大鼠中，测定了给予2-脱氧葡萄糖后血糖和血浆游离脂肪酸的反应。完整大鼠和去传入神经大鼠的肾上腺髓质切除均降低了2-脱氧葡萄糖诱导的血糖升高，但不影响正常大鼠血浆游离脂肪酸对2-脱氧葡萄糖的反应。药物在完整大鼠中诱导的血糖水平升高不受去传入神经支配的显著影响，但与之形成鲜明对比的是，在有肾上腺髓质和无肾上腺髓质的情况下，去传入神经大鼠给予2-脱氧葡萄糖后血浆游离脂肪酸的动员均被完全抑制。这些结果证实了先前的观察结果，表明交感神经系统和肾上腺髓质释放的肾上腺素参与了2-脱氧葡萄糖引起的高血糖症的产生。此外，它们还为在前下丘脑或边缘结构中存在能够通过直接激活脂肪组织的交感纤维而不干预葡萄糖稳态来特异性影响游离脂肪酸动员的中枢提供了证据。双侧下丘脑损伤动物的实验虽然数量不多，但似乎支持上述结论。
