Rosen S G, Clutter W E, Shah S D, Miller J P, Bier D M, Cryer P E
Am J Physiol. 1983 Dec;245(6):E616-26. doi: 10.1152/ajpendo.1983.245.6.E616.
Six normal humans each underwent infusions of 1) saline; 2) propranolol; 3) somatostatin; 4) somatostatin with propranolol; and 5) somatostatin with propranolol plus phentolamine on separate occasions. Propranolol alone had no effect on glucose production or plasma glucose. Somatostatin alone produced the expected initial decrease followed by an increase in both hepatic glucose production and plasma glucose. beta-Adrenergic blockade with propranolol displaced the glucose production (MANOVA, P = 0.0220) and plasma glucose (MANOVA, P = 0.0057) somatostatin response curves to higher levels, whereas alpha-adrenergic blockade with phentolamine combined with beta-adrenergic blockade displaced the glucose production (MANOVA, P = 0.0281) and plasma glucose (MANOVA, P = 0.0134) somatostatin response curves to lower levels. Because plasma insulin, C-peptide, and glucagon were suppressed comparably under all three conditions and plasma glucose concentrations were comparable initially, this represents direct alpha-adrenergic stimulation of hepatic glucose production in postabsorptive humans demonstrable when the primary glucoregulatory hormones are withdrawn and beta-adrenergic mechanisms are blocked. It is best attributed to sympathetic neural norepinephrine release.
1）生理盐水；2）普萘洛尔；3）生长抑素；4）生长抑素与普萘洛尔；5）生长抑素、普萘洛尔加酚妥拉明。单独使用普萘洛尔对葡萄糖生成或血糖没有影响。单独使用生长抑素会使肝葡萄糖生成和血糖先出现预期的下降，随后上升。普萘洛尔的β-肾上腺素能阻滞作用将生长抑素的葡萄糖生成反应曲线（多变量方差分析，P = 0.0220）和血糖反应曲线（多变量方差分析，P = 0.0057）上移至更高水平，而酚妥拉明的α-肾上腺素能阻滞作用与β-肾上腺素能阻滞作用联合使用则将生长抑素的葡萄糖生成反应曲线（多变量方差分析，P = 0.0281）和血糖反应曲线（多变量方差分析，P = 0.0134）下移至更低水平。由于在所有三种情况下血浆胰岛素、C肽和胰高血糖素均受到类似抑制，且最初血浆葡萄糖浓度相当，这表明在吸收后状态的人体中，当主要的葡萄糖调节激素被去除且β-肾上腺素能机制被阻断时，可证明存在对肝葡萄糖生成的直接α-肾上腺素能刺激。这最可能归因于交感神经去甲肾上腺素的释放。
