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大鼠体内游离脂肪酸动员的中枢调节的进一步证据。

Further evidence for a central regulation of free fatty acid mobilization in the rat.

作者信息

Gross J L, Migliorini R H

出版信息

Am J Physiol. 1977 Feb;232(2):E165-71. doi: 10.1152/ajpendo.1977.232.2.E165.

Abstract

Previous studies have shown that anterior hypothalamic deafferentation in rats completely suppresses the increase in plasma free fatty acid (FFA), but not the hyperglycemia induced by administration of 2-deoxyglucose, suggesting a specific central regulation of FFA mobilization. The physiological importance of this finding was further investigated by examining in deafferented rats the response to several stimuli that modify the rate of lipomobilization in normal rats. The results show that the hypothalamic lesion interferes with FFA mobilization mainly when increased sympathetic activity is required: during cold exposure or forced muscular activity, and after insulin-induced hypoglycemia or a relatively long period of fasting. Changes in blood sugar responses, when observed, could be interpreted as secondary to an initial block in FFA mobilization. The data support our hypothesis that there are areas in the central nervous system sensitive to glycopenia and activated in situations requiring rapid mobilization of metabolic reserves that can specifically influence FFA mobilization through an activation of the sympathetic fibers of adipose tissue.

摘要

先前的研究表明,大鼠下丘脑前部去传入神经支配可完全抑制血浆游离脂肪酸(FFA)的升高,但不能抑制2-脱氧葡萄糖给药诱导的高血糖,这表明FFA动员存在特定的中枢调节。通过检查去传入神经大鼠对几种改变正常大鼠脂肪动员速率的刺激的反应,进一步研究了这一发现的生理重要性。结果表明,下丘脑损伤主要在需要增加交感神经活动时干扰FFA动员:在冷暴露或强迫肌肉活动期间,以及胰岛素诱导的低血糖或相对长时间禁食后。观察到的血糖反应变化可解释为FFA动员初始阻滞的继发结果。这些数据支持我们的假设,即中枢神经系统中存在对低血糖敏感的区域,在需要快速动员代谢储备的情况下被激活,可通过激活脂肪组织的交感神经纤维来特异性影响FFA动员。

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