Alterations of irisin, adropin, preptin and BDNF concentrations in coronary heart disease patients comorbid with depression

Abstract

Background: Depression is a well-known co-morbidity of coronary heart disease (CHD) and these two diseases share common risk mechanisms. Here, the aim of this study was to investigate the possible link between energy homeostasis regulation and CHD patients comorbid with depression.Methods: Two hundred and nine CHD patients and 101 matched healthy individuals were included. Demographic, clinical data were collected, serum irisin, adropin, preptin and brain-derived neurotrophic factor (BDNF) levels were determined by a double-antibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA), and the depression was scored by Patient Health Questionnaire-9 (PHQ-9). Correlation analysis as well as multiple linear regression was used to assess the relationship between the three peptides, BDNF serum levels and PHQ-9 scores.Results: Irisin serum level was significantly lower in CHD patients without depression as compared with healthy controls (P=0.002), as well as adropin (P=0.000), preptin (P=0.000) and BDNF (P=0.000). Furthermore, similar trends were observed in CHD patients with depression in terms of irisin, adropin and BDNF as compared with CHD patients without depression (P=0.006; P=0.003; P=0.002; respectively).Multiple logistic regression results confirmed the contribution of irisin and BDNF to the occurrence of depression in CHD. Interestingly, correlations analysis revealed significant negative correlations between PHQ-9 scores and irisin, adropin, BDNF level (r=−0.43, P<0.01; r=−0.29, P<0.05; r=−0.45, P<0.001 respectively), and irisin serum level was positively correlated with BDNF (r=0.38, P<0.01). Conclusions:Our study firstly identified the role of energy homeostasis in the susceptibility to depression in CHD patients, and the interaction between irisin and BDNF could trigger the imbalance of energy homeostasis that occurs in depression of CHD patients.

Adropin as A Fat-Burning Hormone with Multiple Functions—Review of a Decade of Research

“…Additionally, low level of adropin in blood was found to be a coronary atherosclerosis predictor in both healthy and type 2 diabetic patients [22]. Low levels of adropin were also detected in patients with coronary heart diseases [39]. Interestingly, adropin levels in patients with coronary heart diseases are generally lower as compared to individuals who additionally are diagnosed as depressive.…”

“…Interestingly, adropin levels in patients with coronary heart diseases are generally lower as compared to individuals who additionally are diagnosed as depressive. Thus, downregulation of adropin in depression may contribute to impaired energy homeostasis in this disease [39]. Finally, low levels of circulating adropin is the predictor of late saphenous vein graft occlusion [40], suggesting that adropin deficiency may contribute to the pathogenesis of saphenous vein graft disease.…”

Association of Brain-Gut Peptides with Inflammatory Cytokines in Moyamoya Disease

“…The concentrations of VIP, CCK, SST, SP, and inflammatory factors IL-1β, TNF-α, and IL-12 in the serum and CSF were measured using the Quantikine enzymelinked immunosorbent assay (for VIP, CCK, SST, and SP: Sigma-Aldrich, St. Louis, MO, USA; for IL-1β, TNF-α, and IL-12: R&D Systems, Minneapolis, MN, USA) according to the protocol provided by the manufacturer. The details have been described in our previous study [26].…”

A Review of Adropin as the Medium of Dialogue between Energy Regulation and Immune Regulation

“…The nomenclature of adropin is derived from the Latin roots "aduro" and "pinquis," meaning "promoting fat burning," with identical amino acid sequences in humans and mice [1]. At present, the half-life of adropin has still remained elusive, and its half-life may last from several minutes to half an hour, which is similar to other secretory proteins [2]. The biological effects of adropin are mediated through activation of the orphan G protein-coupled receptor 19 (GPR19) [3,4].…”