Laurent D, Petersen K F, Russell R R, Cline G W, Shulman G I
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Am J Physiol. 1998 Jan;274(1):E130-8. doi: 10.1152/ajpendo.1998.274.1.E130.
To examine the effects of a physiological increase in plasma epinephrine concentration (approximately 800 pg/ml) on muscle glycogenolysis and insulin-stimulated glycogenesis, we infused epinephrine [1.2 micrograms.(m2 body surface)-1.min-1] for 2 h and monitored muscle glycogen and glucose 6-phosphate (G-6-P) concentrations with 13C/31P nuclear magnetic resonance (NMR) spectroscopy. Epinephrine caused an increase in plasma glucose (delta approximately 50 mg/dl), lactate (delta approximately 1.4 mM), free fatty acids (delta approximately 1,200 microM at peak), and whole body glucose oxidation (delta approximately 0.85 mg.kg-1.min-1) compared with levels in a group of control subjects (n = 4) in the presence of slight hyperinsulinemia (approximately 13 microU/ml, n = 8) or basal insulin (approximately 7 microU/ml, n = 7). However, epinephrine did not induce any detectable changes in glycogen or G-6-P concentrations, whereas muscle inorganic phosphate (Pi) decreased by 35%. Epinephrine infusion during a euglycemic-hyperinsulinemic clamp (n = 8) caused a 45% decrease in the glucose infusion rate that could be mostly attributed to a 73% decrease in muscle glycogen synthesis rate. After an initial increase to approximately 160% of basal values, G-6-P levels decreased by approximately 30% with initiation of the epinephrine infusion. We conclude that a physiological increase in plasma epinephrine concentration 1) has a negligible effect on muscle glycogenolysis at rest, 2) decreases muscle Pi, which may maintain phosphorylase activity at a low level, and 3) causes a major impairment in insulin-stimulated muscle glycogen synthesis, possibly due to inhibition of glucose transport-phosphorylation activity.
为了研究血浆肾上腺素浓度生理性升高（约800 pg/ml）对肌肉糖原分解及胰岛素刺激的糖原合成的影响，我们以[1.2微克·（平方米体表面积）⁻¹·分钟⁻¹]的速率输注肾上腺素2小时，并用¹³C/³¹P核磁共振（NMR）波谱法监测肌肉糖原和6-磷酸葡萄糖（G-6-P）的浓度。与一组在轻度高胰岛素血症（约13微单位/毫升，n = 8）或基础胰岛素水平（约7微单位/毫升，n = 7）下的对照受试者（n = 4）相比，肾上腺素使血浆葡萄糖（Δ约50毫克/分升）、乳酸（Δ约1.4毫摩尔）、游离脂肪酸（峰值时Δ约1200微摩尔）和全身葡萄糖氧化（Δ约0.85毫克·千克⁻¹·分钟⁻¹）升高。然而，肾上腺素并未引起糖原或G-6-P浓度的任何可检测到的变化，而肌肉无机磷酸盐（Pi）下降了35%。在正常血糖-高胰岛素钳夹期间（n = 8）输注肾上腺素导致葡萄糖输注速率下降45%，这主要归因于肌肉糖原合成速率下降73%。在最初升高至基础值的约160%后，随着肾上腺素输注开始，G-6-P水平下降了约30%。我们得出结论，血浆肾上腺素浓度的生理性升高：1）对静息时的肌肉糖原分解影响可忽略不计；2）降低肌肉Pi，这可能使磷酸化酶活性维持在低水平；3）导致胰岛素刺激的肌肉糖原合成严重受损，可能是由于葡萄糖转运-磷酸化活性受到抑制。
