Newby F D, Wilson L K, Thacker S V, DiGirolamo M
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30303.
Am J Physiol. 1990 Dec;259(6 Pt 1):E865-71. doi: 10.1152/ajpendo.1990.259.6.E865.
The metabolic state occurring with refeeding after fasting is characterized by the rapid restoration of hepatic glycogen. Recent evidence suggests that a main substrate for glycogenesis is lactate. Because adipose tissue is an active site of lactate production that increases with fasting, we examined the magnitude and duration of lactate production by isolated adipocytes from three adipose depots of rats fasted for 48 h and then refed for up to 96 h. The data show that 48 h of fasting results in a markedly elevated rate of adipocyte lactate production, which increased from 3-9% of total glucose metabolized in the fed state to 49-60% in the fasted state. During the refeeding period, lactate production remained elevated for 12-24 h and then declined. Mesenteric adipocytes had a higher rate and more prolonged elevation in lactate production than cells from the other two depots. We conclude that, with refeeding after a fast, adipocyte glucose conversion to lactate remains elevated during the time of hepatic glycogen restoration. This suggests that adipose tissue may actively produce lactate for glycogenesis during refeeding.
禁食后再进食时出现的代谢状态的特征是肝糖原迅速恢复。最近的证据表明，糖原生成的主要底物是乳酸。由于脂肪组织是乳酸产生的活跃部位，且随着禁食而增加，我们研究了从禁食48小时然后再进食长达96小时的大鼠的三个脂肪储存部位分离出的脂肪细胞产生乳酸的量和持续时间。数据显示，禁食48小时会导致脂肪细胞乳酸产生率显著升高，从进食状态下占总葡萄糖代谢量的3 - 9%增加到禁食状态下的49 - 60%。在再进食期间，乳酸产生量在12 - 24小时内保持升高，然后下降。肠系膜脂肪细胞产生乳酸的速率更高，且升高持续时间比其他两个储存部位的细胞更长。我们得出结论，禁食后再进食时，在肝糖原恢复期间，脂肪细胞将葡萄糖转化为乳酸的过程仍然处于升高状态。这表明脂肪组织可能在再进食期间积极产生乳酸用于糖原生成。
