McGuinness O P, Shau V, Benson E M, Lewis M, Snowden R T, Greene J E, Neal D W, Cherrington A D
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232-0615, USA.
Am J Physiol. 1997 Oct;273(4):E674-81. doi: 10.1152/ajpendo.1997.273.4.E674.
The role of epinephrine and norepinephrine in contributing to the alterations in hepatic glucose metabolism during a 70-h stress hormone infusion (SHI) was investigated in four groups of chronically catheterized (20-h-fasted) conscious dogs. SHI increased glucagon (approximately 5-fold), epinephrine (approximately 10-fold), norepinephrine (approximately 10-fold), and cortisol (approximately 6-fold) levels. Dogs received either all the hormones (SHI; n = 5), all the hormones except epinephrine (SHI-Epi; n = 6), or all the hormones except norepinephrine (SHI-NE; n = 6). In addition, six dogs received saline only (Sal). Glucose production (Ra) and gluconeogenesis were assessed after a 70-h hormone or saline infusion with the use of tracer ([3-(3)H]glucose and [U-(14)C]alanine) and arteriovenous difference techniques. SHI increased glucose levels (108 +/- 2 vs. 189 +/- 10 mg/dl) and Ra (2.6 +/- 0.2 vs. 4.1 +/- 0.3 mg x kg(-1) x min(-1)) compared with Sal. The absence of an increase in epinephrine markedly attenuated these changes (glucose and Ra were 140 +/- 6 mg/dl and 2.7 +/- 0.4 mg x kg(-1) x min(-1), respectively). Only 25% of the blunted rise in Ra could be accounted for by an attenuation of the rise in net hepatic gluconeogenic precursor uptake (0.9 +/- 0.1, 1.5 +/- 0.1, and 1.1 +/- 0.2 mg x kg(-1) x min(-1) for Sal, SHI, and SHI-Epi, respectively). The absence of an increase in norepinephrine did not blunt the rise in arterial glucose levels, Ra, or net hepatic gluconeogenic precursor uptake (they rose to 195 +/- 21 mg/dl, 3.7 +/- 0.5 mg x kg(-1) x min(-1), and 1.7 +/- 0.2 mg x kg(-1) min(-1), respectively). In summary, during chronic SHI, the rise in epinephrine exerts potent stimulatory effects on glucose production principally by enhancing hepatic glycogenolysis, although the rise in circulating norepinephrine has minimal effects.
在四组长期插管（禁食20小时）的清醒犬中，研究了肾上腺素和去甲肾上腺素在70小时应激激素输注（SHI）期间对肝脏葡萄糖代谢改变的作用。SHI使胰高血糖素（约5倍）、肾上腺素（约10倍）、去甲肾上腺素（约10倍）和皮质醇（约6倍）水平升高。犬只分别接受所有激素（SHI；n = 5）、除肾上腺素外的所有激素（SHI-Epi；n = 6）或除去甲肾上腺素外的所有激素（SHI-NE；n = 6）。此外，六只犬只仅接受生理盐水（Sal）。在70小时激素或生理盐水输注后，使用示踪剂（[3-(3)H]葡萄糖和[U-(14)C]丙氨酸）和动静脉差值技术评估葡萄糖生成（Ra）和糖异生。与Sal相比，SHI使血糖水平升高（108±2 vs. 189±10 mg/dl）和Ra升高（2.6±0.2 vs. 4.1±0.3 mg·kg⁻¹·min⁻¹）。肾上腺素未升高显著减弱了这些变化（血糖和Ra分别为140±6 mg/dl和2.7±0.4 mg·kg⁻¹·min⁻¹）。Ra的钝化升高中只有25%可归因于肝脏净糖异生前体摄取升高的减弱（Sal、SHI和SHI-Epi分别为0.9±0.1、1.5±0.1和1.1±0.2 mg·kg⁻¹·min⁻¹）。去甲肾上腺素未升高并未减弱动脉血糖水平、Ra或肝脏净糖异生前体摄取的升高（它们分别升至195±21 mg/dl、3.7±0.5 mg·kg⁻¹·min⁻¹和1.7±0.2 mg·kg⁻¹·min⁻¹）。总之，在慢性SHI期间，肾上腺素的升高主要通过增强肝脏糖原分解对葡萄糖生成产生强大的刺激作用，而去甲肾上腺素的升高影响最小。
