French T J, Holness M J, MacLennan P A, Sugden M C
Department of Chemical Pathology, London Hospital Medical College, U.K.
Biochem J. 1988 Mar 15;250(3):773-9. doi: 10.1042/bj2500773.
We examined the long-term effects of nutritional status and the acute effects of changes in exogenous carbohydrate- and lipid-substrate supply and utilization on fructose 2,6-bisphosphate (Fru-2,6-P2) concentrations in heart, gastrocnemius and soleus. Starvation decreased Fru-2,6-P2 concentrations in all three muscles. The acute administration of insulin and glucose increased skeletal-muscle Fru-2,6-P2 in the fed, but not in the starved, state, but cardiac Fru-2,6-P2 was unchanged. Cardiac and skeletal-muscle Fru-2,6-P2 concentrations were unaffected by acute increases in fatty acid supply produced by the administration of corn oil plus heparin, or by acute decreases in fatty acid supply produced by inhibition of lipolysis. Differences in cardiac and skeletal-muscle Fru-2,6-P2 concentrations observed in response to starvation were not reversed by administration of glucose or glucose plus insulin, or by inhibition of lipolysis, even though changes in citrate (heart), acylcarnitine (heart) and glycogen (skeletal muscle) were observed. Concentrations remained low for at least 8 h after chow re-feeding, but the fed value was restored by 24 h.
我们研究了营养状况的长期影响以及外源性碳水化合物和脂质底物供应与利用的变化对心脏、腓肠肌和比目鱼肌中果糖2,6-二磷酸（Fru-2,6-P2）浓度的急性影响。饥饿降低了所有这三块肌肉中的Fru-2,6-P2浓度。在进食状态下，急性给予胰岛素和葡萄糖可增加骨骼肌中的Fru-2,6-P2，但在饥饿状态下则不会，而心脏中的Fru-2,6-P2没有变化。给予玉米油加肝素所导致的脂肪酸供应急性增加，或抑制脂肪分解所导致的脂肪酸供应急性减少，均未影响心脏和骨骼肌中的Fru-2,6-P2浓度。尽管观察到了柠檬酸（心脏）、酰基肉碱（心脏）和糖原（骨骼肌）的变化，但给予葡萄糖或葡萄糖加胰岛素，或抑制脂肪分解，均未逆转饥饿状态下观察到的心脏和骨骼肌Fru-2,6-P2浓度差异。重新喂食食物后，浓度至少在8小时内保持较低水平，但在24小时时恢复到进食时的水平。
