Association between plasma dipeptidyl peptidase-4 activity to brain-derived neurotrophic factor ratio and depressive symptoms in middle-aged and older adults with normal glucose tolerance: A cross-sectional study

Association between plasma dipeptidyl peptidase-4 activity to brain-derived neurotrophic factor ratio and depressive symptoms in middle-aged and older adults with normal glucose tolerance: A cross-sectional study
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糖耐量正常的中老年人血浆二肽基肽酶 4 活性与脑源性神经营养因子比率与抑郁症状的关联:一项横断面研究

DOI:
10.1080/15622975.2020.1733078
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发表时间:
2020-02
期刊:
World J. Biol. Psychiatry
影响因子:
--
通讯作者:
Chen yujie
Chen yujie
中科院分区:
其他
文献类型:
--
作者:
Zheng tianpeng;Chen xu;Ge bo;Chen bo;Qin linyuan;Tian li;Gao yun;Hu xueping;Xiao liuping;Pan haidong;Chen yujie

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摘要目标:脑源性神经营养因子(BDNF)可用性的减弱和二肽基肽酶-4(DPP 4)活性的增加都被报道与抑郁症的发病机制有关。本研究的目的是测试抑郁症状和血浆DPP 4活性与BDNF比率(DBR)之间的相关性。研究方法:我们在1640名非糖尿病参与者的横断面样本中评估了DPP 4活性、BDNF、氧化应激参数和炎症标志物,并计算了DBR。结果:在有和没有抑郁症状的参与者中,DPP 4活性与BDNF呈负相关(r=-0.351和r=-0.404,p<.001)。硝基酪氨酸和8-iso-PGF 2a分别介导了DPP 4活性对BDNF的总效应的18.4%和12.6%。在DBR四分位数中,8-iso-PGF 2a、硝基酪氨酸、C-反应蛋白、白细胞介素-6和PHQ-9评分逐渐增加。DBR处于最高四分位数的参与者有2.64倍的抑郁症状几率(OR = 3.03)。随着BDNF水平的降低和DPP 4活性水平的升高,抑郁症状的风险增加更多(p<0.05)。结论:我们的数据表明,通过氧化应激介导的DPP 4活性和BDNF呈负相关。DBR和抑郁症状风险之间的正相关关系提高了将DBR鉴定为新的生物标记物甚至可能的抑郁症治疗靶点的可行性。
Abstract Objectives: Attenuation of brain-derived neurotrophic factor (BDNF) availability and increased dipeptidyl peptidase-4 (DPP4) activity have both been reported to link to the pathogenesis of depression. The aim of this study was to test the correlation between depressive symptoms and plasma DPP4 activity to BDNF ratio (DBR). Methods: We evaluated DPP4 activity, BDNF, oxidative stress parameters and inflammatory markers and calculated DBR in a cross-sectional sample of 1640 non-diabetic participants. Results: DPP4 activity was negatively related to BDNF in participants with and without depressive symptoms (r= −0.351 and r= −0.404, p<.001). Nitrotyrosine and 8-iso-PGF2a mediated 18.4 and 12.6% of the total effect of DPP4 activity on BDNF, respectively. 8-iso-PGF2a, nitrotyrosine, C-reactive protein, interleukin-6 and PHQ-9 score progressively increased across DBR quartiles. Participants whose DBRs were in the highest quartile had 2.64-fold increased odds (OR = 3.03) of depressive symptoms. The depressive symptoms risk increased more with lower levels of BDNF and higher levels of DPP4 activity (p<.05). Conclusions: Our data suggested inverse correlation between DPP4 activity and BDNF through the oxidative stress mediator. The positive relationship between DBR and depressive symptoms risk raises feasibility of identifying DBR as a novel biological marker or even a possible therapeutic target for depression.
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