Gamaro G D, Prediger M E, Lopes J, Bassani M G, Dalmaz C
Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos 2600, ANEXO Lab 11 CEP: 90035-003, Porto Alegre, Rio Grande do Sul, Brazil.
Pharmacol Biochem Behav. 2008 Sep;90(3):312-7. doi: 10.1016/j.pbb.2008.03.005. Epub 2008 Mar 14.
Stress-induced alterations in feeding behavior are sexually dimorphic and have been related to changes in monoamine levels. Fluoxetine is commonly used as an antidepressant and has also been suggested as an adjunct to other strategies to treat obese individuals. Leptin may interact with stress hormones and with the brain serotonergic system, possibly affecting the feeding behavior of stressed rats. The aim of this study is to evaluate the interaction between chronic fluoxetine treatment and leptin levels in adult female Wistar rats submitted to chronic variable stress. After 30 days of stress, control and stressed groups were subdivided into two groups that received daily injections of vehicle or fluoxetine (8 mg/kg, i.p.). Body weight was evaluated before and after fluoxetine treatment. The animals gained weight with time, signifying that there is a difference in weight gain over time when fluoxetine-treated animals are, or not, subjected to the stress model. Both fluoxetine and stress induced a decrease in sweet food consumption. On the 60th day of fluoxetine treatment, leptin levels were decreased in fluoxetine-treated animals and there was no effect of stress. We conclude that chronic fluoxetine treatment induced a decreased intake of sweet food, as well as a reduction in leptin levels, and that this result could represent a compensatory response to reduced food intake rather than a direct anorectic mechanism. No interaction with chronic stress was observed.
应激诱导的摄食行为改变具有性别差异,且与单胺水平的变化有关。氟西汀常用作抗抑郁药,也被建议作为治疗肥胖个体的其他策略的辅助药物。瘦素可能与应激激素以及大脑血清素能系统相互作用,可能会影响应激大鼠的摄食行为。本研究的目的是评估成年雌性Wistar大鼠在经受慢性可变应激后,慢性氟西汀治疗与瘦素水平之间的相互作用。应激30天后,将对照组和应激组再细分为两组,分别每日注射赋形剂或氟西汀(8毫克/千克,腹腔注射)。在氟西汀治疗前后评估体重。动物体重随时间增加,这表明接受氟西汀治疗的动物是否经受应激模型,体重增加随时间存在差异。氟西汀和应激均导致甜食消耗量减少。在氟西汀治疗的第60天,接受氟西汀治疗的动物瘦素水平降低,应激没有影响。我们得出结论,慢性氟西汀治疗导致甜食摄入量减少以及瘦素水平降低,这一结果可能代表对食物摄入量减少的代偿反应,而非直接的食欲抑制机制。未观察到与慢性应激的相互作用。