Department of Zoology, University of Mysore, Manasagangotri, Mysore, India.
Stress. 2012 May;15(3):262-71. doi: 10.3109/10253890.2011.619604. Epub 2011 Oct 12.
The present study tested the hypothesis that long-term repeated exposure to stressors results in irreversible changes in carbohydrate metabolism. Groups of adult male rats (five per group) were restrained for 1 h and 4 h later were forced to swim for 15 min everyday for 2, 4, or 24 weeks; five rats were autopsied after each interval. Groups of five rats exposed to stress for 2 or 4 weeks were maintained without further treatment (recovery groups) for up to 24 weeks. The fasting blood glucose concentration, measured at weekly intervals, was significantly higher in the stressed rats than in controls throughout the experiment, except in the 24th week, whereas that of the recovery groups was significantly higher than controls only up to the 8th week after the end of stress exposure and then reached normalcy. The blood concentrations of glucose, lactate, and pyruvate were significantly higher in the 2 and 4 weeks stress groups than in controls, whereas, except for lactate, in rats stressed for 24 weeks these values did not significantly differ from those in controls. These changes were accompanied by increased gluconeogenesis and glycogenolysis as shown by alterations in activities of hepatic carbohydrate metabolizing enzymes and unaltered blood insulin concentrations in rats stressed for 2, 4, and 24 weeks. Furthermore, the blood insulin levels did not significantly vary among controls and the 2, 4, and 24 weeks stress groups. The results reveal that though hyperglycemia induced by long-term stress exposure is reversible, it persists for a prolonged period, even after the termination of stress exposure, before reaching normalcy. Prevalence of hyperglycemia for a prolonged period through increased activities of hepatic enzymes in stressed rats exemplifies allostasis.
本研究旨在验证长期反复暴露于应激源会导致碳水化合物代谢发生不可逆变化的假设。成年雄性大鼠（每组 5 只）被束缚 1 小时，随后在接下来的 24 周内，每天被迫游泳 15 分钟，4 小时后；每组有 5 只大鼠在每个时间点进行尸检。暴露于应激 2 或 4 周的 5 只大鼠在无进一步治疗（恢复期）的情况下维持 24 周。在整个实验过程中，除了在第 24 周外，应激大鼠的空腹血糖浓度每周测量一次，显著高于对照组；而恢复期大鼠的空腹血糖浓度仅在应激结束后第 8 周显著高于对照组，然后恢复正常。2 周和 4 周应激组的血糖、乳酸和丙酮酸浓度显著高于对照组，而 24 周应激组的这些值除了乳酸外，与对照组无显著差异。这些变化伴随着糖异生和糖原分解的增加，表现为肝碳水化合物代谢酶活性的改变和应激 2、4 和 24 周大鼠的血胰岛素浓度不变。此外，对照组和应激 2、4 和 24 周大鼠的血胰岛素水平没有显著差异。结果表明，尽管长期应激暴露引起的高血糖是可逆的，但即使在应激暴露结束后，它仍会持续很长一段时间，然后才恢复正常。应激大鼠肝酶活性增加导致的高血糖持续时间延长，体现了适应的概念。
