Department of Psychiatry and Behavioral Neuroscience, Obesity Research Center, Metabolic Disease Institute, University of Cincinnati, 2170 E. Galbraith Rd., Cincinnati, OH 45237, USA.
Am J Physiol Endocrinol Metab. 2011 Aug;301(2):E307-16. doi: 10.1152/ajpendo.00009.2011. Epub 2011 May 3.
Syrian hamsters, like many humans, increase food intake and body adiposity in response to stress. We hypothesized that glucocorticoids (cortisol and corticosterone) mediate these stress-induced effects on energy homeostasis. Because Syrian hamsters are dual secretors of cortisol and corticosterone, differential effects of each glucocorticoid on energy homeostasis were investigated. First, adrenal intact hamsters were injected with varying physiological concentrations of cortisol, corticosterone, or vehicle to emulate our previously published defeat regimens (i.e., 1 injection/day for 5 days). Neither food intake nor body weight was altered following glucocorticoid injections. Therefore, we investigated the effect of sustained glucocorticoid exposure on energy homeostasis. This was accomplished by implanting hamsters with supraphysiological steady-state pellets of cortisol, corticosterone, or cholesterol as a control. Cortisol, but not corticosterone, significantly decreased food intake, body mass, and lean and fat tissue compared with controls. Despite decreases in body mass and adiposity, cortisol significantly increased circulating free fatty acids, triglyceride, cholesterol, and hepatic triglyceride concentrations. Although corticosterone did not induce alterations in any of the aforementioned metabolic end points, Syrian hamsters were responsive to the effects of corticosterone since glucocorticoids both induced thymic involution and decreased adrenal mass. These findings indicate that cortisol is the more potent glucocorticoid in energy homeostasis in Syrian hamsters. However, the data suggest that cortisol alone does not mediate stress-induced increases in food intake or body mass in this species.
叙利亚仓鼠与许多人类一样，在应激反应中会增加食物摄入量和体脂肪量。我们假设糖皮质激素（皮质醇和皮质酮）介导了这些应激对能量平衡的影响。由于叙利亚仓鼠是皮质醇和皮质酮的双重分泌体，因此研究了每种糖皮质激素对能量平衡的差异影响。首先，给肾上腺完整的仓鼠注射不同生理浓度的皮质醇、皮质酮或载体，以模拟我们之前发表的失败方案（即每天注射 1 次，持续 5 天）。糖皮质激素注射后，食物摄入量或体重均未改变。因此，我们研究了持续糖皮质激素暴露对能量平衡的影响。这是通过给仓鼠植入超生理稳态的皮质醇、皮质酮或胆固醇丸（作为对照）来实现的。与对照组相比，皮质醇而非皮质酮显著降低了食物摄入量、体重以及瘦体重和脂肪组织。尽管体重和体脂肪减少，但皮质醇显著增加了循环游离脂肪酸、甘油三酯、胆固醇和肝甘油三酯浓度。尽管皮质酮没有引起上述任何代谢终点的改变，但由于糖皮质激素均诱导胸腺萎缩和肾上腺质量减少，叙利亚仓鼠对皮质酮的作用有反应。这些发现表明，在叙利亚仓鼠中，皮质醇是能量平衡中更有效的糖皮质激素。然而，数据表明，皮质醇本身并不能介导该物种应激诱导的食物摄入量或体重增加。
