Department of Psychiatry and EMGO Institute for Health and Care Research, VU University Medical Center/GGZ inGeest, Amsterdam, The Netherlands; Longitudinal Studies Section, Translational Gerontology Branch, National Institute on Aging, Baltimore, MD, USA.
Department of Medical Humanities and Social Sciences, Florida State University College of Medicine, Tallahassee, FL, USA; Laboratory of Population Science, National Institute on Aging, Baltimore, MD, USA.
Psychoneuroendocrinology. 2014 Apr;42:1-10. doi: 10.1016/j.psyneuen.2013.12.015. Epub 2014 Jan 4.
Evidence for a role of leptin in depression is limited and conflicting. Inconclusive findings may be explained by the complex effect of obesity on leptin signaling. In particular, both hyperleptinemia due to leptin resistance in obese persons as well as low leptin in lean persons can imply that low leptin biological signaling is associated with an increased risk of significant depressive symptoms. We tested whether the relationship between leptin and depressive symptoms is modulated by abdominal adiposity in two population-based studies.
Data were from 851 participants (65-94 years) of the InCHIANTI Study and 1064 (26-93 years) of the Baltimore Longitudinal Study of Aging (BLSA). Plasma concentrations of leptin, waist circumference and depressive symptoms via the Center for Epidemiological Studies-Depression scale (CES-D) were assessed. In longitudinal InCHIANTI analyses onset of depressed mood (CES-D≥20) was evaluated over a 9-year follow-up.
In pooled cross-sectional analyses the interaction between leptin and waist circumference was significantly associated with CES-D scores ((log)leptin-by-waist interaction p=0.01). Also in longitudinal analyses, the (log)leptin-by-waist interaction term significantly (p=0.04) predicted depressed mood onset over time; depressed mood risk was especially increased for high levels of both leptin and waist circumference.
The present findings suggest that low leptin signaling rather than low leptin concentration is a risk factor for depression. Future studies should develop proxy measures of leptin signaling by combining information on abdominal adiposity and leptin level to be used for clinical and research applications.
瘦素在抑郁症中的作用的证据有限且相互矛盾。肥胖对瘦素信号的复杂影响可能解释了不确定的研究结果。具体来说，肥胖人群中由于瘦素抵抗导致的高瘦素血症以及瘦人群体中的低瘦素血症都意味着低瘦素生物学信号与发生严重抑郁症状的风险增加有关。我们在两项基于人群的研究中测试了瘦素与抑郁症状之间的关系是否受腹部肥胖的调节。
数据来自 InCHIANTI 研究的 851 名参与者（65-94 岁）和巴尔的摩纵向衰老研究（BLSA）的 1064 名参与者（26-93 岁）。通过流行病学研究中心抑郁量表（CES-D）评估了血浆瘦素浓度、腰围和抑郁症状。在纵向 InCHIANTI 分析中，评估了 9 年随访期间出现抑郁情绪（CES-D≥20）的情况。
在汇总的横断面分析中，瘦素和腰围之间的相互作用与 CES-D 评分显著相关（（log）leptin-by-waist 相互作用 p=0.01）。在纵向分析中，（log）leptin-by-waist 交互项也显著（p=0.04）预测了随着时间的推移出现抑郁情绪；对于瘦素和腰围都处于高水平的个体，发生抑郁情绪的风险尤其增加。
本研究结果表明，低瘦素信号而不是低瘦素浓度是抑郁的危险因素。未来的研究应该通过结合腹部肥胖和瘦素水平的信息来开发瘦素信号的替代指标，用于临床和研究应用。
