Smith D M, Fuller S J, Sugden P H
Biochem J. 1986 Jun 1;236(2):543-7. doi: 10.1042/bj2360543.
Compared with glucose, lactate + acetate stimulated ventricular protein synthesis in anterogradely perfused hearts from fed or 72 h-starved rats. Stimulation was greater on a percentage basis in starved rats. Atrial protein synthesis was not detectably stimulated by lactate + acetate. Insulin stimulated protein synthesis in atria and ventricles. The stimulation of protein synthesis by lactate + acetate and insulin was not additive, the percentage stimulation by insulin being less in the ventricles of lactate + acetate-perfused hearts than in glucose-perfused hearts. Perfusion of hearts from 72 h-starved or alloxan-diabetic rats with glucose + lactate + acetate + insulin did not increase protein-synthesis rates or efficiencies (protein synthesis expressed relative to total RNA) to values for fed rats, implying there is a decrease in translational activity in these hearts. In the perfused heart, inhibition of protein synthesis by starvation and its reversal by re-feeding followed a relatively prolonged time course. Synthesis was still decreasing after 3 days of starvation and did not return to normal until after 2 days of re-feeding.
与葡萄糖相比,乳酸盐+醋酸盐可刺激进食大鼠或饥饿72小时大鼠经顺行灌注心脏的心室蛋白合成。以百分比计算,饥饿大鼠的刺激作用更强。乳酸盐+醋酸盐对心房蛋白合成未检测到刺激作用。胰岛素可刺激心房和心室的蛋白合成。乳酸盐+醋酸盐与胰岛素对蛋白合成的刺激作用并非相加的,在乳酸盐+醋酸盐灌注心脏的心室中,胰岛素的刺激百分比低于葡萄糖灌注心脏。用葡萄糖+乳酸盐+醋酸盐+胰岛素灌注饥饿72小时或四氧嘧啶糖尿病大鼠的心脏,并未使蛋白合成速率或效率(相对于总RNA的蛋白合成)提高到进食大鼠的水平,这意味着这些心脏的翻译活性降低。在灌注心脏中,饥饿对蛋白合成的抑制及其通过重新进食的逆转过程相对较长。饥饿3天后合成仍在下降,直到重新进食2天后才恢复正常。