Moore M C, Rossetti L, Pagliassotti M J, Monahan M, Venable C, Neal D, Cherrington A D
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232, USA.
Am J Physiol. 1996 Aug;271(2 Pt 1):E215-22. doi: 10.1152/ajpendo.1996.271.2.E215.
The role of the liver nerves in the disposition of peripherally administered glucose was examined in seven hepatic innervated (HI) and nine hepatic denervated (HD) 42-h-fasted conscious dogs. After a 40-min basal period, there was a 4-h experimental period during which the hepatic glucose load was increased twofold via peripheral glucose infusion. Somatostatin was infused to suppress pancreatic endocrine secretion, and insulin and glucagon were infused intraportally to produce a fourfold increase in insulin and a gradual decrease (approximately 25%) in glucagon. The area under the curve of net hepatic glucose uptake (NHGU) during the glucose infusion period totaled 483 +/- 82 and 335 +/- 32 mg/kg in HD and HI, respectively (P < 0.05). The area under the curve of the hepatic fractional extraction of glucose was 27% greater in HD (P < 0.05). Net hepatic lactate output was similar in the two groups, and net hepatic glycogen synthesis was 3.8 +/- 0.8 vs. 2.7 +/- 0.5 mg.kg dog wt-1.min-1 in HD and HI, respectively (P = 0.13). The direct pathway of glycogen synthesis was responsible for 54-58% of net hepatic glycogen synthesis in both HI and HD (n = 6 for both). In summary 1) NHGU in response to peripheral glucose infusion was approximately 44% greater in HD than in HI, 2) net hepatic glycogen synthesis was enhanced by 41% in HD although the probability of this change was 0.13, and 3) the contribution of the direct pathway to glycogen synthesis was the same in HD and HI. These data are consistent with a role for the liver nerves in regulating the magnitude of NHGU in response to glucose administration. They also indicate that the absence of liver nerves may reduce glycogen turnover during glucose infusion.
在7只具有肝神经支配（HI）和9只肝去神经支配（HD）的42小时禁食清醒犬中，研究了肝神经在外周给予葡萄糖处置过程中的作用。在40分钟的基础期后，进入4小时的实验期，在此期间通过外周输注葡萄糖使肝脏葡萄糖负荷增加两倍。输注生长抑素以抑制胰腺内分泌分泌，并经门静脉输注胰岛素和胰高血糖素，使胰岛素增加四倍，胰高血糖素逐渐降低（约25%）。在葡萄糖输注期，HD组和HI组肝脏净葡萄糖摄取（NHGU）曲线下面积分别总计为483±82和335±32mg/kg（P<0.05）。HD组肝脏葡萄糖分数提取曲线下面积大27%（P<0.05）。两组肝脏乳酸净输出相似，HD组和HI组肝脏糖原净合成分别为3.8±0.8与2.7±0.5mg·kg犬体重-1·min-1（P=0.13）。糖原合成的直接途径在HI组和HD组中均占肝脏糖原净合成的54%-58%（两组n均为6）。总之，1）HD组对外周葡萄糖输注的反应中，NHGU比HI组大约高44%；2）HD组肝脏糖原净合成增加了41%，尽管这种变化的可能性为0.13；3）直接途径对糖原合成的贡献在HD组和HI组中相同。这些数据与肝神经在调节对葡萄糖给药的NHGU幅度中的作用一致。它们还表明，肝神经缺失可能会减少葡萄糖输注期间的糖原周转。
