Role of hepatic alpha- and beta-adrenergic receptor stimulation on hepatic glucose production during heavy exercise.
Role of hepatic alpha- and beta-adrenergic receptor stimulation on hepatic glucose production during heavy exercise.
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剧烈运动期间肝脏α-和β-肾上腺素能受体刺激对肝葡萄糖产生的作用。
DOI：
10.1152/ajpendo.1997.273.5.e831
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Wasserman,DH
中科院分区：
文献类型：
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作者：
Coker,RH;Krishna,MG;Lacy,DB;Bracy,DP;Wasserman,DH
采用选择性阻断肝脏α-和β-肾上腺素能受体的技术，研究了犬在剧烈运动过程中儿茶酚胺在控制肝脏葡萄糖生成中的作用。在研究前>16天进行手术，此时将导管植入颈动脉、门静脉和肝静脉中用于取样，并植入门静脉和腔静脉中用于输注。此外，在门静脉和肝动脉上植入流量探头。每项研究均包括100分钟的平衡、30分钟的基础运动、20分钟的剧烈运动（最大心率的0.85%）、30分钟的恢复和30分钟的肾上腺素能阻滞测试期。门静脉输注生理盐水（对照;n= 7）或α（酚妥拉明）和β（普萘洛尔）肾上腺素能阻滞剂（Blk;n= 6）。在两组中，在阻断试验期间，在门静脉中输注肾上腺素（Epi）和去甲肾上腺素（NE），以在肝脏中产生超生理水平。同位素（[3- 3 H]葡萄糖）稀释和动静脉差异用于评估肝功能。两组运动期间动脉Epi、NE、胰高血糖素和胰岛素水平相似。在运动过程中，对照组和Blk组的内源性葡萄糖生成（Ra）在时间= 20 min时相似地升高至7.9 ± 1.2和7.5 ± 2.0 mg·kg-1·min-1。对照组和Blk组的净肝葡萄糖输出也在运动中升高至相似的速率。在阻断试验期间，动脉血糖和拉糖分别降至164 ± 5 mg/dl和12.0 ± 1.4 mg·kg-1·min-1，但Blk组基本不变。Blk对儿茶酚胺输注的减弱反应证实了肝肾上腺素能阻滞的有效性。总之，这些结果表明，直接的肝肾上腺素能刺激不参与增加Ra，即使在夸张的交感神经反应剧烈运动。
The role of catecholamines in the control of hepatic glucose production was studied during heavy exercise in dogs, using a technique to selectively block hepatic α- and β-adrenergic receptors. Surgery was done >16 days before the study, at which time catheters were implanted in the carotid artery, portal vein, and hepatic vein for sampling and the portal vein and vena cava for infusions. In addition, flow probes were implanted on the portal vein and hepatic artery. Each study consisted of a 100-min equilibration, a 30-min basal, a 20-min heavy exercise (∼85% of maximum heart rate), a 30-min recovery, and a 30-min adrenergic blockade test period. Either saline (control;n= 7) or α (phentolamine)- and β (propranolol)-adrenergic blockers (Blk;n= 6) were infused in the portal vein. In both groups, epinephrine (Epi) and norepinephrine (NE) were infused in the portal vein during the blockade test period to create supraphysiological levels at the liver. Isotope ([3-3H]glucose) dilution and arteriovenous differences were used to assess hepatic function. Arterial Epi, NE, glucagon, and insulin levels were similar during exercise in both groups. Endogenous glucose production (Ra) rose similarly during exercise to 7.9 ± 1.2 and 7.5 ± 2.0 mg ⋅ kg−1⋅ min−1in control and Blk groups at time = 20 min. Net hepatic glucose output also rose to a similar rate in control and Blk groups with exercise. During the blockade test period, arterial plasma glucose and Rarose to 164 ± 5 mg/dl and 12.0 ± 1.4 mg ⋅ kg−1⋅ min−1, respectively, but were essentially unchanged in Blk. The attenuated response to catecholamine infusion in Blk substantiates the effectiveness of the hepatic adrenergic blockade. In conclusion, these results show that direct hepatic adrenergic stimulation does not participate in the increase in Ra, even during the exaggerated sympathetic response to heavy exercise.