Ricart-Jané David, Rodríguez-Sureda Victor, Benavides Alex, Peinado-Onsurbe Julia, López-Tejero M Dolores, Llobera Miquel
Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain.
Metabolism. 2002 Jul;51(7):925-31. doi: 10.1053/meta.2002.33353.
In humans, stress can increase the risk of cardiovascular disease by altering lipoprotein metabolism. Scarce experimental and clinical data are available on this effect. Therefore, we studied the metabolic response to acute and chronic stress following a model of immobilization (IMO) in rats and we evaluated the resulting circulating lipoprotein levels. Repeated IMO treatment (2 hours daily, always between 9:00 AM and 11:00 AM, for 2 periods of 5 and 4 consecutive days, separated by 2 days of rest) daily decreased body weight gain and food intake, increased adrenal weight, and slightly reduced liver glycogen and plasma insulin (without considerable variations of blood glucose), which is characteristic of chronic stress. A single IMO application (30 minutes of an unexpected IMO starting at 2:00 PM immediately before the animals were killed) significantly increased the circulating levels of corticosterone, glucose, insulin, glycerol, and ketone bodies, which is the typical response to acute stress. Both acute and chronic stress decreased the plasmatic triacylglycerol (TAG) concentration, as reflected by the reduction in the number of very-low-density lipoprotein (VLDL) particles. This may be due to an increase in the metabolization of TAG, as suggested by the slightly higher amounts of circulating LDLs. Chronic stress, but not acute stress, significantly increased both the number and the estimated size of circulating high-density lipoprotein (HDLs), as shown by the plasma cholesterol concentration. Acute stress did not have an additive effect over chronic stress on the lipoprotein parameters studied. The metabolic effects of these IMO-induced alterations on lipoprotein profiles are discussed, and future studies in lipidic metabolism are suggested.
在人类中,压力可通过改变脂蛋白代谢增加心血管疾病风险。关于这种效应的实验和临床数据稀缺。因此,我们采用大鼠固定模型(IMO)研究了急性和慢性应激后的代谢反应,并评估了由此产生的循环脂蛋白水平。重复进行IMO处理(每天2小时,总是在上午9:00至11:00之间,连续5天和4天各进行2个周期,中间休息2天),每日体重增加和食物摄入量降低,肾上腺重量增加,肝糖原和血浆胰岛素略有减少(血糖无显著变化),这是慢性应激的特征。单次进行IMO处理(在动物处死前立即于下午2:00开始意外IMO处理30分钟)显著增加了皮质酮、葡萄糖、胰岛素、甘油和酮体的循环水平,这是急性应激的典型反应。急性和慢性应激均降低了血浆三酰甘油(TAG)浓度,这通过极低密度脂蛋白(VLDL)颗粒数量的减少得以体现。这可能是由于TAG代谢增加所致,循环中低密度脂蛋白(LDL)量略高表明了这一点。如血浆胆固醇浓度所示,慢性应激而非急性应激显著增加了循环高密度脂蛋白(HDL)的数量和估计大小。急性应激对所研究的脂蛋白参数没有叠加于慢性应激的效应。讨论了这些IMO诱导的改变对脂蛋白谱的代谢影响,并提出了脂质代谢方面的未来研究方向。