Ladrière L, Malaisse W J
Laboratory of Experimental Medicine, Brussels Free University, Brussels, Belgium.
Cell Biochem Funct. 2000 Sep;18(3):153-60. doi: 10.1002/1099-0844(200009)18:3<153::AID-CBF858>3.0.CO;2-Q.
This study was designed to assess the effect of the dimethyl ester of succinic acid (SAD) upon the hormonal and metabolic response to a 60-min exercise in overnight-starved Goto-Kakizaki rats. Twenty Goto-Kakizaki rats were starved overnight and then either maintained at rest or obliged to swim for 60 min. Half of the rats were injected intraperitoneally with the dimethyl ester of succinic acid (SAD, 5.0 micromol g(-1) body wt) immediately before exercise (or 60 min of rest). In the hereditarily diabetic rats, overnight starvation lowered the plasma D- glucose, insulin and lactate concentrations, while increasing that of free fatty acids and beta-hydroxybutyrate. In resting rats, the injection of SAD increased the glycogen content of liver, heart and muscle and the plasma concentration of D-glucose, insulin, glycerol and free fatty acids. In control animals, not injected with SAD, exercise increased the plasma concentration of D- glucose, lactate and glycerol, whilst lowering both that of insulin and the glycogen content of liver, heart and muscle. The injection of SAD before exercise failed to prevent and, on occasion, even accentuated the changes in both the glycogen content of liver, heart and muscle and the plasma concentration of D-glucose, insulin, glycerol and free fatty acids, whilst minimizing the increase in lactate concentration otherwise caused by exercise. Nevertheless, the comparison between resting and exercising rats, both injected with SAD, suggested that the ester abolished the exercise-induced rise in D-glucose, glycerol and fatty acid concentrations. By comparison with comparable experiments conducted in overnight-starved normal rats, these findings emphasize both the difference between normal and diabetic rats in their metabolic response to exercise, especially in terms of changes in glycemia, and the usefulness of SAD to compensate for the increased consumption of endogenous nutrients during exercise.
本研究旨在评估琥珀酸二甲酯（SAD）对过夜禁食的Goto-Kakizaki大鼠在60分钟运动时激素和代谢反应的影响。20只Goto-Kakizaki大鼠过夜禁食，然后要么保持静止，要么被迫游泳60分钟。一半的大鼠在运动前（或休息60分钟）立即腹腔注射琥珀酸二甲酯（SAD，5.0微摩尔/克体重）。在遗传性糖尿病大鼠中，过夜禁食降低了血浆D-葡萄糖、胰岛素和乳酸浓度，同时增加了游离脂肪酸和β-羟基丁酸的浓度。在静止的大鼠中，注射SAD增加了肝脏、心脏和肌肉的糖原含量以及血浆D-葡萄糖、胰岛素、甘油和游离脂肪酸的浓度。在未注射SAD的对照动物中，运动增加了血浆D-葡萄糖、乳酸和甘油的浓度，同时降低了胰岛素浓度以及肝脏、心脏和肌肉的糖原含量。运动前注射SAD未能预防，有时甚至加剧了肝脏、心脏和肌肉糖原含量以及血浆D-葡萄糖、胰岛素、甘油和游离脂肪酸浓度的变化，同时将运动否则会引起的乳酸浓度增加降至最低。然而，对均注射了SAD的静止和运动大鼠的比较表明，该酯消除了运动诱导的D-葡萄糖、甘油和脂肪酸浓度的升高。与在过夜禁食的正常大鼠中进行的类似实验相比，这些发现强调了正常大鼠和糖尿病大鼠在运动代谢反应方面的差异，尤其是在血糖变化方面，以及SAD在补偿运动期间内源性营养物质消耗增加方面的作用。
