John Curtin School of Medical Research, College of Health and Medicine, Australian National University, Canberra, ACT, 0200, Australia.
Section on Neural Gene Expression, National Institute of Mental Health, Building 49, Room 5A51, 49 Convent Drive, Bethesda, MD, 20892, USA.
Transl Psychiatry. 2019 Jan 16;9(1):10. doi: 10.1038/s41398-018-0351-z.
Antidepressants are among the most-prescribed class of drugs in the world and though weight gain is a common outcome of antidepressant treatment, that effect is not well understood. We employed an animal model comprised of 2 weeks of chronic restraint stress with antidepressant treatment, followed by diet-induced obesity. We showed that short-term antidepressant treatment had long-lasting effects, not only leading to weight gain, but also enhancing trabecular and cortical bone features in rats; therefore, weight gain in this model was different from that of the classic diet-induced obesity. Late in the post-restraint recovery period, antidepressant-treated animals were significantly heavier and had better bone features than saline-treated controls, when assessed in the distal femoral metaphysis. The propensity to gain weight might have influenced the rate of catch-up growth and bone allometry, as heavier animals treated with fluoxetine also had enhanced bone features when compared to non-stressed animals. Therefore, short-term antidepressant treatment ameliorated the long-term effects of stress on body growth and bone. Growth and bone structural features were associated with leptin levels, and the interaction between leptin levels and antidepressant was significant for bone mineral content, suggesting that short-term antidepressants in the context of long-term diet-induced obesity modified the role of leptin in bone formation. To our knowledge this is the first study reporting that short-term antidepressant treatment has long-lasting effects in restoring the effects of chronic stress in body weight and bone formation. Our findings may be relevant to the understanding and treatment of osteoporosis, a condition of increasing prevalence due to the aging population.
抗抑郁药是世界上最常开的药物之一,尽管体重增加是抗抑郁治疗的常见后果,但这种影响尚不清楚。我们采用了一种动物模型,该模型包括 2 周的慢性束缚应激和抗抑郁治疗,随后进行饮食诱导肥胖。我们表明,短期抗抑郁治疗具有持久的效果,不仅导致体重增加,而且增强了大鼠的小梁骨和皮质骨特征;因此,该模型中的体重增加与经典的饮食诱导肥胖不同。在束缚恢复期后期,与生理盐水处理的对照组相比,接受抗抑郁药治疗的动物体重明显增加,且骨特征更好,在股骨远端干骺端进行评估时情况如此。体重增加的趋势可能会影响追赶生长和骨比例的速度,因为与非应激动物相比,接受氟西汀治疗的体重较重的动物的骨特征也得到了增强。因此,短期抗抑郁治疗改善了应激对身体生长和骨骼的长期影响。生长和骨骼结构特征与瘦素水平相关,瘦素水平与抗抑郁药之间的相互作用对骨矿物质含量有显著影响,这表明在长期饮食诱导肥胖的情况下,短期抗抑郁药改变了瘦素在骨形成中的作用。据我们所知,这是第一项报道短期抗抑郁治疗具有持久作用,可恢复慢性应激对体重和骨形成的影响的研究。我们的发现可能与骨质疏松症的理解和治疗有关,随着人口老龄化,骨质疏松症的患病率不断增加。