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Purpose: Soluble vascular adhesion protein-1 (sVAP-1) and adropin are 2 biomarkers of endothelial dysfunction. The main purpose of this study was to evaluate the levels of sVAP-1 in patients with moderate and severe obstructive sleep apnea (OSA) compared to healthy controls, and to further determine the relationship between sVAP-1 and adropin levels, as well as inflammatory biomarkers and sleep parameters. Methods: In this study, we included 50 male patients with OSA (25 moderate and 25 severe) and 20 age- and sex-matched control subjects. Patients with OSA underwent polysomnography. All subjects underwent fasting peripheral blood sampling for laboratory analysis. Results: Serum sVAP-1 and inflammatory biomarkers (IL-6, TNF-α, and hsCRP) levels were significantly higher in patients with severe OSA compared to those with moderate OSA and control groups, while plasma levels of adropin showed the opposite trend. Furthermore, sVAP-1 levels had a significant positive correlation with AHI, ODI, TNF-α, IL-6, and hsCRP levels and a significant negative correlation with adropin levels. The receiver operating characteristic analysis showed an Area Under Curve (AUC) of.876 (P <.001) for sVAP-1 levels predicting OSA. Serum sVAP-1 threshold of > 445.5 ng/mL had an 88% sensitivity and 80% specificity for detecting OSA status. Multivariate regression analysis demonstrated that sVAP-1 remained a significant positive predictor of OSA severity. Conclusions: Increased sVAP-1 levels in OSA patients are significantly correlated with indices of OSA severity, adropin levels, and inflammatory biomarkers, suggesting that sVAP-1 plays a vital role in the pathophysiology of OSA and may become a potential screening tool in the evaluation of OSA severity. [ABSTRACT FROM AUTHOR]

Macrophage polarization is increasingly recognized as a vital pathogenetic factor in Crohn's disease (CD). Adropin is a secreted protein implicated in energy homeostasis, chiefly linked to glucose and lipid metabolism. However, the significance of adropin in CD is not clear. The objective of this study was to detect the expression of adropin in CD patients and investigate the effect of adropin on macrophage polarization induced by lipopolysaccharide (LPS) and its potential mechanism. Our study showed that serum adropin levels were markedly lower in patients with CD in active (CDA) than patients with CD in remission (CDR) and control groups (p < 0.01), however, there was no significant difference between in remission CD and healthy controls (p > 0.05). The colon mucous adropin levels in CDA were distinctly higher than CDR and controls (p < 0.01), while a significant difference between in remission CD and in healthy controls was not observed (p > 0.05). Exploration of the specific mechanism of action indicated that adropin promoted LPS‐induced RAW264.7 macrophage polarization to M2 phenotype by modulating the expression and nuclear translocation of peroxisome proliferator receptor gamma (PPARγ), which may help weaken the intestinal inflammatory response. PPARγ inhibitor GW9662 reversed adropin‐induced M2 macrophage polarization. Knockdown of GPR19, an adropin receptor, abrogated the M2 macrophage polarization caused by PPARγ. These findings suggest that adropin in colonic mucosa is a protective response in patients with active Crohn's disease. [ABSTRACT FROM AUTHOR]

Objective: Adropin is a unique hormone, which controls metabolism and energy homeostasis. Hyperthyroidism is a disease with a high metabolic rate that affects both glucose and lipid metabolism. We aimed to investigate the change of adropin levels and the association between adropin levels and clinical parameters in patients with hyperthyroidism. Methods: This cross‐sectional study comprised 90 newly diagnosed patients with hyperthyroidism and 90 age‐ and gender‐matched healthy controls. Circulating adropin levels and thyroid hormone levels were evaluated in each participant. Results: Compared with the healthy controls, the hyperthyroid patients had significantly higher levels of serum adropin (p < 0.001). In addition, adropin levels were positively correlated with free triiodothyronine (FT3) and free thyroxine (FT4), whereas they were negatively correlated with thyroid‐stimulating hormone (TSH). A multivariate linear regression analysis showed that serum adropin concentrations were independently correlated with FT3 and TSH after adjustment for age, gender, and other confounding factors (FT3: β = 0.231, p < 0.05; TSH: β = −0.301, p < 0.05). Conclusions: Patients with hyperthyroidism had elevated serum adropin levels. And the serum adropin concentrations were independently correlated with the FT3 and TSH levels. [ABSTRACT FROM AUTHOR]

Background: In recent years, there has been a lot of discussion over the impact of ultra-processed foods (UPFs) intake on overall health of subjects. However, the association between UPFs intake and metabolic unhealthy (MU) status is still in a state of ambiguity. The current study assessed the relationship between UPFs intake and MU status with regard to brain-derived neurotrophic factor (BDNF) and adropin levels. Methods: A sample of Iranian adults (aged 20–65 years) was selected to participate in this cross-sectional study using a multistage cluster random-sampling method. UPFs intake was assessed by a validated food frequency questionnaire and NOVA classification. Concentrations of metabolic parameters, BDNF and adropin were determined through fasting blood samples. MU status was assessed according to the criteria proposed by Wildman. Results: The overall prevalence of MU phenotype among study participants (n = 527) was 42.5%. Higher intake of UPFs was associated with elevated odds of MU status in multivariable-adjusted model (ORT3 vs. T1=1.88; 95%CI: 1.02–3.45). Moreover, a positive association was observed between UPFs intake and hypertriglyceridemia after controlling all confounders (ORT3 vs. T1=2.07; 95%CI: 1.15–3.73). However, each tertile increase in UPFs intake was not significantly associated with serum BDNF ( =0.15; 95%CI: -0.05, 0.34; P = 0.14) and adropin ( =-1.37; 95%CI: -6.16, 3.42; P = 0.58) levels in multivariable-adjusted linear regression models. Conclusion: Our findings suggested that higher consumption of UPFs was related to increased likelihood of MU status among a sample of Iranian adults. Further longitudinal studies are needed to verify the directionality and generalizability of the results to all adult populations. [ABSTRACT FROM AUTHOR]

Purpose: Adropin is an emerging metabolic hormone that has a role in regulating energy homeostasis. The present study aimed to explore the impact of adropin on redox homeostasis and its possible role in testicular functions in adult mouse testis. Methods: Western blot, flow-cytometry, and TUNEL assay were performed to explore the impact of intra-testicular treatment of adropin (0.5 μg/testis) on testicular functions of adult mice. Hormonal assay was done by ELISA. Further, antioxidant enzyme activities were measured. Results: Adropin treatment significantly increased the sperm count and testicular testosterone by increasing the expression of GPR19 and steroidogenic proteins. Also, adropin treatment reduced the oxidative/nitrosative stress by facilitating the translocation of NRF2 and inhibiting NF-κB into the nucleus of germ cells. Enhanced nuclear translocation of NRF2 leads to elevated biosynthesis of antioxidant enzymes, evident by increased HO-1, SOD, and catalase activity that ultimately resulted into declined LPO levels in adropin-treated mice testes. Furthermore, adropin decreased nuclear translocation of NF-κB in germ cells, that resulted into decreased NO production leading to decreased nitrosative stress. Adropin/GPR19 signaling significantly increased its differentiation, proliferation, and survival of germ cells by elevating the expression of PCNA and declining caspase 3, cleaved caspase 3 expression, Bax/Bcl2 ratio, and TUNEL-positive cells. FACS analysis revealed that adropin treatment enhances overall turnover of testicular cells leading to rise in production of advanced germ cells, notably spermatids. Conclusion: The present study indicated that adropin improves testicular steroidogenesis, spermatogenesis via modulating redox potential and could be a promising target for treating testicular dysfunctions. [ABSTRACT FROM AUTHOR]

Background: Alterations in the circulating concentrations and target-tissue action of organokines underpin the development of insulin resistance in microgravity and gravity deprivation. The purpose of this study was to examine changes in circulating adropin, irisin, retinol binding protein-4 (RBP4), and the metabolic response of healthy young males following 60 days of 6° headdown-tilt (HDT) bed rest, with and without reactive jump training (RJT), to explore links with whole-body and tissue-specific insulin sensitivity. To our knowledge, this is the first time that adropin, irisin, and RBP4 have been studied in HDT bed rest. Methods: A total of 23 male subjects (29 ± 6 years, 181 ± 6 cm, 77 ± 7 kg) were exposed to 60 days of 6° HDT bed rest and randomized to a control (CTRL, n = 11) or a RJT (JUMP, n = 12) group (48 sessions with =4 min total training time per session). Circulating adropin, irisin, and RBP4 were quantified in fasting serum before and after HDT bed rest. A subanalysis was performed a posteriori to investigate individual metabolic responses post-HDT bed rest based on subjects that showed an increase or decrease in whole-body insulin sensitivity (Matsuda index). Results: There were significant main effects of time, but not group, for decreases in adropin, irisin, Matsuda index, and liver insulin sensitivity following HDT bed rest (p < 0.05), whereas RBP4 did not change. The subanalysis identified that in a subgroup with decreased whole-body insulin sensitivity (n = 17), RBP4 increased significantly, whereas adropin, irisin, and liver insulin sensitivity were all decreased significantly following HDT bed rest. Conversely, in a subgroup with increased whole-body insulin sensitivity (n = 6), liver insulin sensitivity increased significantly after HDT bed rest, whereas adropin, irisin, and RBP4 did not change. Conclusion: Investigating individual metabolic responses has provided insights into changes in circulating adropin, irisin, RBP4, in relation to insulin sensitivity following HDT bed rest. We conclude that adropin, irisin, and RBP4 are candidate biomarkers for providing insights into whole-body and tissue-specific insulin sensitivity to track changes in physiological responsiveness to a gravity deprivation intervention in a lean male cohort. [ABSTRACT FROM AUTHOR]

Diabetes mellitus affects 537 million adults around the world. Adropin is expressed in different cell types. Our aim was to investigate the cellular localization in the endocrine pancreas and its effect on modulating pancreatic endocrine hormone release in streptozotocin (STZ)-induced diabetic rats. Adropin expression in the pancreas was investigated in normal and diabetic rats using immunohistochemistry and immunoelectron microscopy. Serum levels of insulin, glucagon pancreatic polypeptide (PP), and somatostatin were measured using a Luminex® χMAP (Magpix®) analyzer. Pancreatic endocrine hormone levels in INS-1 832/3 rat insulinoma cells, as well as pancreatic tissue fragments of normal and diabetic rats treated with different concentrations of adropin (10−6, 10−9, and 10−12 M), were measured using ELISA. Adropin was colocalized with cells producing either insulin, glucagon, or PP. Adropin treatment reduced the number of glucagon-secreting alpha cells and suppressed glucagon release from the pancreas. The serum levels of GLP-1 and amylin were significantly increased after treatment with adropin. Our study indicates a potential role of adropin in modulating glucagon secretion in animal models of diabetes mellitus. [ABSTRACT FROM AUTHOR]

The current study aimed to evaluate the serum levels of nitric oxide (NO) and adropin in males with non-alcoholic fatty liver disease (NAFLD) induced erectile dysfunction (ED) and NAFLD patients without ED and controls. The current study selected 165 participants from the hepatology department from November 2021 to November 2022. The patients were either suffering from NAFLD with normal liver functions or non-alcoholic steatohepatitis with abnormal liver functions. They were diagnosed by abdominal ultrasonography. Participants were evaluated using the validated Arabic version of the International Index of Erectile Function (ArIIEF-5), the Arabic form of the Generalized Anxiety Disorder-7 (GAD-7) questionnaire and the Patient Health Questionnaire-9 (PHQ-9). Noteworthy, there were significant positive correlations between ArIIEF-5 score, NO, adropin and total testosterone (r = 0.380, p = 0.001; r = 0.507, p = < 0.001; r = 0.246, p = 0.038, respectively). Meanwhile, there were significant negative correlations between ArIIEF-5 score, creatinine, duration of the disease and scores of GAD-7 and PHQ-9 (r = -0.656, p = < 0.001; r = -0.368, p = 0.002; r = -0.663, p = < 0.001; r = -0.248, p = 0.037, respectively). Finally, a linear regression analysis revealed that GAD-7, creatinine, and adropin were the only strong independent predictors of ArIIEF-5, as the 95% confidence interval in the form of upper and lower bounds was -0.349, -0.843, p < 0.001, -6.507, -18.402, p < 0.001, 0.476, 0.117, and p 0.002, respectively. Impaired NO and adropin levels play a potential role in the development of ED in patients with NAFLD. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction (ED) plays a prominent role in the pathogenesis of preeclampsia (PE). There is a need for non-invasive methods to assess endothelial function in preeclamptic patients. In the present study, adropin, autotaxin (ATX), and lysophosphatidic acid (LPA) were evaluated as indicators of ED. Patients diagnosed with PE and healthy pregnant women (n = 42 for each group) were compared. After measuring flow-mediated dilation (FMD), the participants were stratified as ED (+) or ED (−) based on a cut-off value of 6.5%. The PE patients were divided as early/late onset PE and severe/mild PE. Adropin, ATX, and LPA levels were measured, and their relevance to ED was evaluated. Student t, Mann–Whitney U, or ANOVA tests were used for statistics, as appropriate. Adropin levels were diminished in the ED (+) group, whereas ATX and LPA levels were increased. The decrease in adropin levels was more pronounced in severe PE, showing a positive correlation with the FMD. In the logistic regression model, adropin was the only parameter that was an independent variable for the FMD test (P <.001). Adropin measurements in serum may be of value for disease follow-up in patients with PE. [ABSTRACT FROM AUTHOR]

Abstract Background In recent years, there has been a lot of discussion over the impact of ultra-processed foods (UPFs) intake on overall health of subjects. However, the association between UPFs intake and metabolic unhealthy (MU) status is still in a state of ambiguity. The current study assessed the relationship between UPFs intake and MU status with regard to brain-derived neurotrophic factor (BDNF) and adropin levels. Methods A sample of Iranian adults (aged 20–65 years) was selected to participate in this cross-sectional study using a multistage cluster random-sampling method. UPFs intake was assessed by a validated food frequency questionnaire and NOVA classification. Concentrations of metabolic parameters, BDNF and adropin were determined through fasting blood samples. MU status was assessed according to the criteria proposed by Wildman. Results The overall prevalence of MU phenotype among study participants (n = 527) was 42.5%. Higher intake of UPFs was associated with elevated odds of MU status in multivariable-adjusted model (ORT3 vs. T1=1.88; 95%CI: 1.02–3.45). Moreover, a positive association was observed between UPFs intake and hypertriglyceridemia after controlling all confounders (ORT3 vs. T1=2.07; 95%CI: 1.15–3.73). However, each tertile increase in UPFs intake was not significantly associated with serum BDNF ( $$\:\beta\:$$ =0.15; 95%CI: -0.05, 0.34; P = 0.14) and adropin ( $$\:\beta\:$$ =-1.37; 95%CI: -6.16, 3.42; P = 0.58) levels in multivariable-adjusted linear regression models. Conclusion Our findings suggested that higher consumption of UPFs was related to increased likelihood of MU status among a sample of Iranian adults. Further longitudinal studies are needed to verify the directionality and generalizability of the results to all adult populations.

Background and Aim: The prevalence of overweight and obesity is increasing dramatically due to unhealthy lifestyles. This study aimed to determine the effects of six weeks of total-body resistance exercise (TRX) combined with purslane supplementation on serum levels of brain-derived neurotrophic factor (BDNF), adropin, and nesfatin in overweight girls. Methods: In this semi-experimental study, 32 overweight female students aged 16 to 18 years (BMI > 25) from Ganaveh County, Bushehr Province, Iran, were randomly selected. The participants were divided into four groups: exercise, supplement, exercise + supplement, and placebo. The exercise groups performed TRX exercises consisting of 9 to 11 movements for six weeks, with three sessions per week, each lasting 60 minutes. Purslane supplementation was administered as two 500 mg capsules of purslane (Perpin Ala) taken daily after breakfast and lunch. Serum levels of BDNF, adropin, and nesfatin were measured using ELISA at the beginning and end of the six-week study. Results: The serum levels of BDNF in the exercise + supplement group showed significant differences compared to the exercise, supplement, and control groups (P < 0.05). Additionally, the serum levels of nesfatin were significantly different between the exercise + supplement group and the control group (P < 0.05). However, there were no significant differences in serum levels of adropin among the groups (P > 0.05). Conclusion: The findings suggest that a combination of TRX exercises and purslane supplementation over six weeks positively affects BDNF and nesfatin levels in young girls, potentially aiding in weight reduction. Further research is needed to explore this area more comprehensively.

We aimed to investigate the relationship among proprotein convertase subtilisin/kexin type 9 (PCSK9), adropin levels, inflammation, and sleep variables in non-diabetic males with severe obstructive sleep apnea (OSA).

Erectile dysfunction (ED) is associated with endothelial damage, especially atherosclerosis. The search for biomarkers that can predict ED still continues. Adropin is known to affect nitric oxide (NO) bioavailability and energy homeostasis. In our study, we have aimed to investigate the relationship between serum adropin levels and ED. Male patients with and without ED between 40–60 years of age, who presented to the outpatient clinics of urology between November 2019–February 2020, were prospectively included in the study. Biochemical values measured at the time of admission to the outpatient clinic. According to the International Index of Erectile Function-5 (IIEF-5) scores which range between 5 and 25 points, patients with a score ≤21 were considered to have ED. The patients were divided into two groups: as ED and non-ED control groups. Laboratory values obtained at admission to outpatient clinics of urology were compared between groups. Patients with (n: 40), and without (n: 40) ED were included in the study. The mean age (50.2 ± 5.7 years), average body mass index (BMI) (29.7 ± 2.5 kg/m2), IIEF score (15.8 ± 6 pts), serum adropin (584.8 ± 172 pg/mL), and total testosterone (396.4 ± 91.7 ng/dL) levels were recorded. Serum adropin and testosterone levels were statistically significantly higher in the non-ED group than in the ED group (712.3 ± 222 pg/mL vs. 511.1 ± 145 pg/mL, p < 0.001 and 420.5 ± 56 ng/dL vs. 374.3 ± 98 ng/dL, respectively p = 0.032). Whereas fasting blood glucose (FBG) values were found to be statistically significantly higher in the ED group (100.2 ± 14 mg/dL vs. 143.8 ± 78 mg/dL, p = 0.001). According to the results of our study, serum levels of adropin which improves endothelial functions were comparatively lower in ED patients, as expected.

Abstract Background Inflammatory bowel disease (IBD) is a chronic relapsing inflammatory disorder of unknown etiology and unpredictable course. The aim of the work was to assess the levels of adropin, fibroblast growth factor-1 (FGF-1), and Toll-like receptor-1 (TLR1) biomarkers in IBD patients compared to controls and evaluate the gene expression of TNF-α as a marker of disease severity. Methods Adropin, fasting serum FGF-1 levels, TLR1, and TNF-α were measured in 60 IBD patients. They were also compared with 58 healthy controls matching age and gender. Moreover, the blood cells cDNA copy number of TNF-α were determined as a marker of severity. Results Adropin and TLR1 levels were significantly lower in patients than controls. FGF-1 was reduced but not statistically significant. The expression of TNF-α gene in the IBD patients was significantly increased (42%) in comparison with control samples (P

In patients with type 2 diabetes mellitus (T2DM), asymptomatic adverse cardiac remodeling plays a pivotal role in the development of heart failure (HF). Patients with T2DM often have low or near-normal levels of natriuretic peptides, including N-terminal brain natriuretic peptide (NT-proBNP), which have been inconclusive in predicting the transition from asymptomatic adverse cardiac remodeling to HF with preserved ejection fraction (HFpEF). The aim of this study was to elucidate the predictive ability of adropin for HFpEF depending on the circulating levels of NT-proBNP. We prospectively enrolled 561 T2DM patients (glycated hemoglobin < 6.9%) with echocardiographic evidence of structural cardiac abnormalities and left ventricular ejection fractions >50%. All patients underwent B-mode transthoracic echocardiographic and Doppler examinations. Circulating biomarkers, i.e., NT-proBNP and adropin, were assessed at baseline. All individuals were divided into two groups according to the presence of low levels (<125 pmol/mL; n = 162) or elevated levels (≥125 pmol/mL; n = 399) of NT-proBNP. Patients with known asymptomatic adverse cardiac remodeling and elevated NT-proBNP were classified as having asymptomatic HFpEF. A multivariate logistic regression showed that low serum levels of adropin (<3.5 ng/mL), its combination with any level of NT-proBNP, and use of SGLT2 inhibitors were independent predictors of HFpEF. However, low levels of adropin significantly increased the predictive ability of NT-proBNP for asymptomatic HFpEF in patients with T2DM, even though the concentrations of NT-proBNP were low, while adropin added discriminatory value to all concentrations of NT-proBNP. In conclusion, low levels of adropin significantly increase the predictive ability of NT-proBNP for asymptomatic HFpEF in patients with T2DM. [ABSTRACT FROM AUTHOR]

Growing evidence supports the role of gut microbiota in chronic inflammation, insulin resistance (IR) and sex hormone production in polycystic ovary syndrome (PCOS). Adropin plays a pivotal role in the regulation of glucose and lipid metabolism and is negatively correlated with IR, which affects intestinal microbiota and sex hormones. However, the effect of adropin administration in PCOS has yet to be investigated. The present study aimed to assess the effects of adropin on letrozole (LTZ)‐induced PCOS in rats and the potential underlying mechanisms. The experimental groups were normal, adropin, letrozole and LTZ + adropin. At the end of the experiment, adropin significantly ameliorated PCOS, as evidenced by restoring the normal ovarian structure, decreasing the theca cell thickness in antral follicles, as well as serum testosterone and luteinizing hormone levels and luteinizing hormone/follicle‐stimulating hormone ratios, at the same time as increasing granulosa cell thickness in antral follicles, oestradiol and follicle‐stimulating hormone levels. The ameliorating effect could be attributed to its effect on sex hormone‐binding globulin, key steroidogenic genes STAR and CYP11A1, IR, lipid profile, gut microbiota metabolites–brain–ovary axis components (short chain fatty acids, free fatty acid receptor 3 and peptide YY), intestinal permeability marker (zonulin and tight junction protein claudin‐1), lipopolysaccharides/Toll‐like receptor 4/nuclear factor kappa B inflammatory pathway and oxidative stress makers (malondialdehyde and total antioxidant capacity). In conclusion, adropin has a promising therapeutic effect on PCOS by regulating steroidogenesis, IR, lipid profile, the gut microbiota inflammatory axis and redox homeostasis. Key points: Adropin treatment reversed endocrine and ovarian morphology disorders in polycystic ovary syndrome (PCOS).Adropin regulated the ovarian steroidogenesis and sex hormone‐binding globulin in PCOS.Adropin improved lipid profile and decreased insulin resistance in PCOS.Adropin modulated the components of the gut–brain–ovary axis (short chain fatty acids, free fatty acid receptor 3 and peptide YY) in PCOS.Adropin improved intestinal barrier integrity, suppressed of lipopolysaccharides/Toll‐like receptor 4/nuclear factor kappa B signalling pathway and oxidative stress in PCOS. [ABSTRACT FROM AUTHOR]

Adropin—a multifunctional peptide with tissue-protective capacity that regulates energy homeostasis, sensitivity to insulin and inflammatory response—seems to show an inverse association with the presence of cardiovascular and renal diseases, obesity and diabetes mellitus in the general population. The purpose of the study is to elucidate whether adropin may be a plausible predictive biomarker for clinical outcomes in post-ST elevation of myocardial infarction (STEMI) patients with newly diagnosed prediabetes according to the American Diabetes Association criteria. A total of 1214 post-STEMI patients who received percutaneous coronary intervention were identified in a local database of the private hospital "Vita Center" (Zaporozhye, Ukraine). Between November 2020 and June 2024, we prospectively enrolled 498 patients with prediabetes in this open prospective cohort study and followed them for 3 years. The combined clinical endpoint at follow-up was defined as cardiovascular death due to acute myocardial infarction, heart failure, sudden death due to arrhythmia or cardiac surgery, and/or all-cause death. We identified 126 clinical events and found that serum levels of adropin < 2.15 ng/mL (area under the curve = 0.836; 95% confidence interval = 0.745–0.928; sensitivity = 84.9%; specificity = 72.7%; likelihood ratio = 3.11; p = 0.0001) predicted clinical outcomes. Multivariate logistic regression showed that a Gensini score ≥ 32 (Odds ratio [OR] = 1.07; p = 0.001), adropin ≤ 2.15 ng/mL (OR = 1.18; p = 0.001), use of SGLT2i (OR = 0.94; p = 0.010) and GLP-1 receptor agonist (OR = 0.95; p = 0.040) were independent predictors of clinical outcome. Kaplan–Meier plots showed that patients with lower adropin levels (≤2.15 ng/mL) had worse clinical outcomes compared to patients with higher adropin levels (>2.15 ng/mL). In conclusion, low levels of adropin (≤2.15 ng/mL) independently predicted clinical outcomes in post-STEMI patients with newly detected prediabetes and improved the discriminative ability of the Gensini score for 3-year follow-up events. Future clinical studies are needed to clarify whether adropin is a promising molecule to be incorporated into conventional risk scores for the prediction of MACCEs after STEMI. [ABSTRACT FROM AUTHOR]

[Display omitted] • Adropin increases eNOS expression in experimental subarachnoid hemorrhage. • Adropin reduces neurobehavioral deficits in experimental subarachnoid hemorrhage. • Adropin reduces oxidative stress in experimental subarachnoid hemorrhage. • Adropin reduces apoptosis in experimental subarachnoid hemorrhage. Purpose: We aimed to investigate early effects of exogenously administered adropin (AD) on neurological function, endothelial nitric oxide synthase (eNOS) expression, nitrite/nitrate levels, oxidative stress, and apoptosis in subarachnoid hemorrhage (SAH). Methods: Following intracerebroventricular AD administration (10 µg/5 µl at a rate of 1 µl/min) SAH model was carried out in Sprague–Dawley rats by injection of autologous blood into the prechiasmatic cistern. The effects of AD were assessed 24 h following SAH. The modified Garcia score was employed to evaluate functional insufficiencies. Adropin and caspase-3 proteins were measured by ELISA, while nitrite/nitrate levels, total antioxidant capacity (TAC) and reactive oxygen/nitrogen species (ROS/RNS) were assayed by standard kits. eNOS expression and apoptotic neurons were detected by immunohistochemical analysis. Results: The SAH group performed notably lower on the modified Garcia score compared to sham and SAH + AD groups. Adropin administration increased brain eNOS expression, nitrite/nitrate and AD levels compared to SHAM and SAH groups. SAH produced enhanced ROS/RNS generation and reduced antioxidant capacity in the brain. Adropin boosted brain TAC and diminished ROS/RNS production in SAH rats and no considerable change amongst SHAM and SAH + AD groups were detected. Apoptotic cells were notably increased in intensity and number after SAH and were reduced by AD administration. Conclusions: Adropin increases eNOS expression and reduces neurobehavioral deficits, oxidative stress, and apoptotic cell death in SAH model. Presented results indicate that AD provides protection in early brain injury associated with SAH. [ABSTRACT FROM AUTHOR]

Introduction: Inactivity and sedentary are of the most important health problems that can affect serum proteins. The present research was conducted with aim to investigate the effect of eight weeks of high-intensity interval training (HIIT) along with the consumption of thyme suplementation on the serum levels of adropin and Tumour Necrosis Factor alpha (TNF-a) in sedentary young girls. Methods: In this quasi-experimental study conducted in 2023, 48 sedentary young girls with mean age of 20.00±1.61 years were randomly divided into four groups: HIIT, thyme, HIIT+thyme and control. Venous blood was taken in the pre-test and post-test stages. Serum levels of adropin and TNF-a were analyzed using specific ELISA kits. The data was analyzed by SPSS statistical software (version 22) using ANOVA and paired t tests. P<0.05 was considered statistically significant. Results: There was no significant difference between the studied groups in the serum level of adropin before the test (P=0.501) and after the test (P=0.732), and the changes in adropin were not significant in the studied groups (P>0.05). A significant decrease in TNF-a values was observed in the thyme (P=0.001) and HIIT thyme groups (P=0.014) after the interventions, while a significant increase in TNF-a values was observed in the HIIT group (P=0.007). Conclusion: Performing HIIT exercises increases TNF-a levels and consuming thyme supplements decreases it and in cases where they are used at the same time, the effect of thyme is still stronger. Adropin levels were not affected by exercise or thyme supplementation. [ABSTRACT FROM AUTHOR]

Background: Inflammatory bowel disease (IBD) is a chronic relapsing inflammatory disorder of unknown etiology and unpredictable course. The aim of the work was to assess the levels of adropin, fibroblast growth factor-1 (FGF-1), and Toll-like receptor-1 (TLR1) biomarkers in IBD patients compared to controls and evaluate the gene expression of TNF-α as a marker of disease severity. Methods: Adropin, fasting serum FGF-1 levels, TLR1, and TNF-α were measured in 60 IBD patients. They were also compared with 58 healthy controls matching age and gender. Moreover, the blood cells cDNA copy number of TNF-α were determined as a marker of severity. Results: Adropin and TLR1 levels were significantly lower in patients than controls. FGF-1 was reduced but not statistically significant. The expression of TNF-α gene in the IBD patients was significantly increased (42%) in comparison with control samples (P < 0.001). Conclusions: Adropin, IGF-I, and Toll-like receptor-1 biomarkers may have a role in the intricate pathophysiology of IBD and may possibly operate as predictors of disease activity. Thus, they may be therapeutic targets for IBD. Moreover, the expression of TNF-α gene can be used as a marker of severity. [ABSTRACT FROM AUTHOR]

• Exercise protects rats from hypertension. • Pomegranate juice (PJ) has beneficial effects on hypertension. • Exercise and PJ increase serum adropin levels. • Adropin negatively correlates with systolic and diastolic pressures. • Exercise and PJ partially reduce oxidative stress caused by hypertension. Hypertension, characterized by persistent and uncontrolled high blood pressure, is one of the most common significant causes of mortality worldwide. Lifestyle modifications such as exercise and antioxidant intake have showed beneficial effects on hypertensive conditions. Adropin and endothelin-1 (ET-1) have important vasoregulatory functions in the endothelium. However, the underlying mechanisms linking exercise- and/or antioxidant intake–mediated improvement of hypertension are not fully understood. In this study, it was hypothesized that swimming exercise and pomegranate juice (PJ) (as an antioxidant) administration might have protective effects on hypertension development and possible involvements of serum adropin and ET-1. To test the hypothesis, the rats with hypertension, induced by Nω-nitro-L-arginine methyl ester hydrochloride, were subjected to swimming exercise and received PJ for 8 weeks. Weekly systolic and diastolic pressures, serum concentrations of adropin and ET-1, and oxidant/antioxidant parameters in various tissues were measured. The obtained data show that swimming exercise leads to complete protection against hypertension within the 8-week duration, whereas the PJ administration causes an ameliorative effect. In addition, the combination of swimming exercise and PJ administration do not have additive effects in protection against hypertension. Notably, the 8-week swimming exercise restores the diminished serum adropin concentration in rats with hypertension to the control level. Serum adropin significantly correlated with systolic and diastolic pressures, depending on swimming exercise, but not PJ administration. Serum ET-1 concentration inconsistently fluctuates in response to Nω-nitro-L-arginine methyl ester hydrochloride, swimming exercise, and PJ intake. In addition, swimming exercise and/or PJ administration lead to a complete normalization in liver malondialdehyde concentrations of rats with hypertension, whereas these interventions cause slight or no improvements in superoxide dismutase, catalase, and glutathione in the heart, liver, and kidney. In conclusion, 8-week swimming exercise modulates hypertension, possibly by influencing adropin concentration and oxidative stress. Hypertension is characterized by persistent and mostly uncontrolled high blood pressure. Adropin is proposed to have important vasoregulatory functions. In this study, exercise completely protects rats from hypertension, whereas pomegranate juice has ameliorative effects on hypertension. Serum adropin may have a role in the protection of hypertension. Abbreviation: L-NAME, Nω-nitro-L-arginine methyl ester hydrochloride. [Display omitted] [ABSTRACT FROM AUTHOR]

There is a lack of evidence on dietary intake of methyl donor nutrients with metabolic health status and related biomarkers. Thus, this study aimed to assess the relation between methyl donor nutrients intake and metabolic health status with regarding the interactive roles of brain-derived neurotrophic factor (BDNF) and adropin in Iranian adults. This cross-sectional survey was conducted among 527 Iranian adults (45.7% female) selected by multistage cluster random-sampling method. A validated food frequency questionnaire was used to evaluate participants' dietary intake. Metabolic unhealthy status was defined by Wildman criteria as having ≥ 2 of hyperglycemia, hypertriglyceridemia, hypo-HDL-cholesterolemia, hypertension, chronic inflammation, and insulin resistance. Concentrations of metabolic parameters, BDNF and adropin were determined using fasting blood samples. An inverse association was found between methyl donor nutrients intake and metabolically unhealthy status in multivariable-adjusted model (OR T3 vs. T1 = 0.30; 95%CI: 0.12–0.75). This association was especially significant among overweight/obese adults and was stronger in women. Additionally, consumption of vitamin B6 and choline was separately related to reduced odds of metabolically unhealthy status. Methyl donor intake was not significantly related to low BDNF (OR T3 vs. T1 = 0.93; 95%CI: 0.60–1.44) and adropin (OR T3 vs. T1 = 0.71; 95%CI: 0.44–1.15). However, the interaction between high methyl donor nutrients intake and high BDNF was related to lower odds of metabolically unhealthy status in multivariable-adjusted model (OR MDNS∗BDNF = 0.27; 95%CI: 0.11–0.67). Higher intake of methyl donor nutrients, alone and in interaction with BDNF levels, was associated with decreased odds of metabolically unhealthy status in Iranian adults. [ABSTRACT FROM AUTHOR]

BackgroundAlterations in the circulating concentrations and target-tissue action of organokines underpin the development of insulin resistance in microgravity and gravity deprivation. The purpose of this study was to examine changes in circulating adropin, irisin, retinol binding protein-4 (RBP4), and the metabolic response of healthy young males following 60 days of 6° head-down-tilt (HDT) bed rest, with and without reactive jump training (RJT), to explore links with whole-body and tissue-specific insulin sensitivity. To our knowledge, this is the first time that adropin, irisin, and RBP4 have been studied in HDT bed rest.MethodsA total of 23 male subjects (29 ± 6 years, 181 ± 6 cm, 77 ± 7 kg) were exposed to 60 days of 6° HDT bed rest and randomized to a control (CTRL, n = 11) or a RJT (JUMP, n = 12) group (48 sessions with ≤4 min total training time per session). Circulating adropin, irisin, and RBP4 were quantified in fasting serum before and after HDT bed rest. A subanalysis was performed a posteriori to investigate individual metabolic responses post-HDT bed rest based on subjects that showed an increase or decrease in whole-body insulin sensitivity (Matsuda index).ResultsThere were significant main effects of time, but not group, for decreases in adropin, irisin, Matsuda index, and liver insulin sensitivity following HDT bed rest (p < 0.05), whereas RBP4 did not change. The subanalysis identified that in a subgroup with decreased whole-body insulin sensitivity (n = 17), RBP4 increased significantly, whereas adropin, irisin, and liver insulin sensitivity were all decreased significantly following HDT bed rest. Conversely, in a subgroup with increased whole-body insulin sensitivity (n = 6), liver insulin sensitivity increased significantly after HDT bed rest, whereas adropin, irisin, and RBP4 did not change.ConclusionInvestigating individual metabolic responses has provided insights into changes in circulating adropin, irisin, RBP4, in relation to insulin sensitivity following HDT bed rest. We conclude that adropin, irisin, and RBP4 are candidate biomarkers for providing insights into whole-body and tissue-specific insulin sensitivity to track changes in physiological responsiveness to a gravity deprivation intervention in a lean male cohort.

Abstract Background Cardiovascular events and poor quality of life are frequently observed in patients with coronary slow flow phenomenon (CSFP). This trial evaluated the effect of nano-curcumin supplement containing curcuminoids, as multifunctional nutraceuticals, on angina status, and some traditional and novel cardiovascular risk factors in overweight or obese patients with CSFP. Methods In this double-blind, randomized, placebo-controlled clinical trial, 42 overweight or obese patients with CSFP received either 80 mg/day of nano-curcumin or placebo for 12 weeks. Seattle angina questionnaire (SAQ) as a clinical measure of angina status, circulating endocan, adropin, homocysteine, lipid profile, and the novel scores of visceral adiposity index (VAI) and waist-triglyceride index (WTI) were assessed before and after the intervention. The independent samples t-test, Mann-Whitney test, analysis of covariance, Chi-square, and Fisher’s exact tests were used where appropriate. Results All domains of SAQ including physical limitation, angina stability, angina frequency-severity, treatment satisfaction, and disease perception and quality of life improved significantly in the nano-curcumin compared with the placebo group. No significant changes were observed in serum endocan, adropin, and homocysteine following the intervention. Triglycerides, triglyceride/high-density lipoprotein cholesterol ratio, WTI and VAI values improved significantly only within the nano-curcumin group. Conclusions Supplementation with 80 mg/day nano-curcumin (containing curcuminoids) for 12 weeks significantly improved clinically important disease-specific aspects of health in patients with CSFP. Some traditional and novel cardiovascular risk factors improved significantly only compared with the baseline values, which need further investigation. Trial registration This study was approved by the Ethics Committee of Tehran University of Medical Sciences (IR.TUMS.VCR.REC.1398.794). The study protocol was registered at Iranian Registry of Clinical Trials by IRCT20131125015536N8 registration ID at 19.06.2019.

Abstract Purpose Our objective was to compare the serum Adropin levels between patients with wet-type Age-Related Macular Degeneration (AMD) and otherwise healthy individuals. Method The study included 45 patients with wet-type AMD and 45 individuals without age-related macular degeneration. Patients with co-morbidities such as diabetes, hypertension, autoimmune diseases, and a previous history of visual impairment; were excluded. FBS, Hemoglobin A1C (HbA1C), lipid profile, and serum Adropin level were checked. Results The mean serum Adropin level of patients with wet-type AMD was significantly lower than the control group (P-value

Background: Cardiovascular events and poor quality of life are frequently observed in patients with coronary slow flow phenomenon (CSFP). This trial evaluated the effect of nano-curcumin supplement containing curcuminoids, as multifunctional nutraceuticals, on angina status, and some traditional and novel cardiovascular risk factors in overweight or obese patients with CSFP. Methods: In this double-blind, randomized, placebo-controlled clinical trial, 42 overweight or obese patients with CSFP received either 80 mg/day of nano-curcumin or placebo for 12 weeks. Seattle angina questionnaire (SAQ) as a clinical measure of angina status, circulating endocan, adropin, homocysteine, lipid profile, and the novel scores of visceral adiposity index (VAI) and waist-triglyceride index (WTI) were assessed before and after the intervention. The independent samples t-test, Mann-Whitney test, analysis of covariance, Chi-square, and Fisher's exact tests were used where appropriate. Results: All domains of SAQ including physical limitation, angina stability, angina frequency-severity, treatment satisfaction, and disease perception and quality of life improved significantly in the nano-curcumin compared with the placebo group. No significant changes were observed in serum endocan, adropin, and homocysteine following the intervention. Triglycerides, triglyceride/high-density lipoprotein cholesterol ratio, WTI and VAI values improved significantly only within the nano-curcumin group. Conclusions: Supplementation with 80 mg/day nano-curcumin (containing curcuminoids) for 12 weeks significantly improved clinically important disease-specific aspects of health in patients with CSFP. Some traditional and novel cardiovascular risk factors improved significantly only compared with the baseline values, which need further investigation. Trial registration: This study was approved by the Ethics Committee of Tehran University of Medical Sciences (IR.TUMS.VCR.REC.1398.794). The study protocol was registered at Iranian Registry of Clinical Trials by IRCT20131125015536N8 registration ID at 19.06.2019. [ABSTRACT FROM AUTHOR]

Introduction: Evidence suggests a link between serum adropin levels and coagulation factors, with physical activity boosting adropin circulation. This study investigates the correlation between adropin and blood coagulation factors in young adults at varying activity levels. Material & Methods: Fifty healthy young adults were divided into active and inactive groups using the Baecke questionnaire. Blood samples assessed adropin and coagulation factors. Statistical tests included Mann-Whitney and independent t-tests for comparison, with Spearman's correlation coefficient determining strength. Results: Active participants exhibited significantly lower fibrinogen (p<0.05) and higher adropin levels (p<0.05) compared to inactive peers. Physical activity correlated negatively (r=-0.27, p=0.05) with fibrinogen but not with adropin and other coagulation factors. Conclusion: Elevated physical activity levels correlate with heightened serum adropin and reduced serum fibrinogen. Moreover, serum fibrinogen, a critical coagulation factor influencing blood clot formation, appears particularly sensitive to the effects of physical activity. [ABSTRACT FROM AUTHOR]

Purpose: Our objective was to compare the serum Adropin levels between patients with wet-type Age-Related Macular Degeneration (AMD) and otherwise healthy individuals. Method: The study included 45 patients with wet-type AMD and 45 individuals without age-related macular degeneration. Patients with co-morbidities such as diabetes, hypertension, autoimmune diseases, and a previous history of visual impairment; were excluded. FBS, Hemoglobin A1C (HbA1C), lipid profile, and serum Adropin level were checked. Results: The mean serum Adropin level of patients with wet-type AMD was significantly lower than the control group (P-value < 0.001). Also, the mean High-sensitivity C-reactive protein (hsCRP) level and High Density Lipoprotein (HDL) were significantly higher in wet-type AMD patients (P-value = 0.031 and < 0.001 respectively). Conclusions: In our study, wet-type AMD was associated with a lower level of serum Adropin. Because of Adropin involvement in glucose metabolism and age-related changes, it may have a role in the pathogenesis of AMD, but it requires more investigations at the molecular level to elucidate its function. [ABSTRACT FROM AUTHOR]

Background: Little is known about the relationship between dietary intake of phytochemicals with metabolic health status and underlying mechanisms. Objectives: Little is known about the relationship between dietary intake of phytochemicals with metabolic health status and underlying mechanisms. We hypothesized that dietary phytochemical index (DPI) improves metabolic health status by ameliorating serum concentrations of brain-derived neurotrophic factor (BDNF) and adropin. Methods: A cross-sectional study was performed in 527 adults (286 males and 241 females). The dietary intakes of participants were collected by a 168-item food frequency questionnaire, and DPI was estimated as a percentage of energy intake derived from phytochemicalrich foods. Anthropometric variables, blood pressure, glycemic and lipid profiles, and biochemical variables were assessed. The metabolically unhealthy (MU) phenotype was determined based on the definition presented by Wildman et al. Results: The MU phenotype was identified in 51.4% of male and 32.0% of female participants. Participants in the third tertile of DPI had 59% lower odds of MU than those in the first tertile (OR: 0.41; 95% CI: 0.19, 0.87) after considering potential confounders. Stratified analysis by sex and body mass index indicated that DPI was inversely related to MU phenotype in females (OR: 0.28; 95% CI: 0.08, 0.97) and normal-weight individuals (OR: 0.11; 95% CI: 0.02, 0.62). DPI was also inversely associated with hyperglycemia, hypertriglyceridemia, and chronic inflammation. Nonsignificant reduced odds of low BDNF (OR: 0.87; 95% CI: 0.42, 1.84) and adropin (OR: 0.75; 95% CI: 0.31, 1.79) were observed in individuals in the top tertile of DPI compared with those in the bottom tertile. Conclusions: This study showed that individuals with higher dietary intake of phytochemicals had lower odds of MU, particularly females and normal-weight individuals. No significant relationship was observed between serum BDNF and adropin with phytochemical intake. [ABSTRACT FROM AUTHOR]

Abstract The present study aimed to investigate the association of nutrient patterns (NPs) with metabolic health status and serum levels of brain-derived neurotrophic factor (BDNF) and adropin in Iranian adults. This cross-sectional survey was performed on 527 adults aged 20–60 years in Isfahan, Iran. To evaluate dietary intake, a validated 168-item semi-quantitative food frequency questionnaire (FFQ) was used. Participants were categorized as metabolically healthy (MH) and metabolically unhealthy (MU) according to their glycemic and lipid profile, insulin resistance (IR), and inflammation status. An overnight fasting blood sample was collected from each participant and serum levels of BDNF and adropin were assessed. A total of 42.50% of participants were recognized as MU. Three NPs were recognized by factor analysis that labeled as “high animal protein” (NP1), “high vegetable” (NP2), and “high carbohydrate” (NP3) patterns. Moderate adherence to NP2 was related to a lower risk of MU (ORT2 vs. T1 = 0.38, 95% CI: 0.18–0.76). Moreover, high adherence of NP2 (T3 vs. T1) was inversely associated with hypertriglyceridemia (OR = 0.27, 95% CI: 0.11–0.65; P-trend

Objective: There is escalating evidence suggesting the beneficial effects of ellagic acid (EA) on the cardiovascular system. The aim of the present study was to investigate the protective effect of EA in human umbilical vein endothelial cells (HUVECs) against high glucose (HG)- induced endothelial dysfunction and to study the potential roles of adropin and nitric oxide (NO) in this regard.Materials and Methods: The experimental groups consisted of normal and HG (30 mM, 48 hr)-treated HUVECs incubated without or with 5 or 10 μM of EA (6 groups of at least 6 replicates, each). The cell count and viability were studied. Moreover, the markers of the redox state, including malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and catalase enzymes, and ferric reducing anti-oxidant power (FRAP), were assayed. The levels of adropin and eNOS gene expression were also studied using RT-qPCR.Results: A high concentration of glucose reduced cell count and caused lipid peroxidation, reduced anti-oxidant capacity of the cells, decreased NO levels, and downregulated the expression of NOS3 (encoding eNOS) and ENHO (encoding adropin) genes. Ellagic acid reversed all these effects.Conclusion: These results suggest a significant protective effect for EA against HG-induced injury in HUVECs. The improved redox state and upregulation of NOS3 and ENHO genes seem to play critical roles in this regard.

Introduction: Energy homeostasis as a metabolic control pathway can be investigated from different dimensions. The present study aimed to assess the effect of eight weeks of aerobic and resistance training on adropin, spexin, and TNFa, as well as insulin resistance indices, in obese men with type 2 diabetes. Material & Methods: In this quasi-experimental study, 30 obese men with type 2 diabetes in khoy in 2022 were selected and randomly assigned to three groups: control, aerobic exercise, and resistance exercise. Aerobic and resistance training (three sessions per week) was performed for eight weeks. In the pre-test and post-test stages, the levels of serum adropin, spexin, and TNFa, as well as the indices of insulin resistance and insulin sensitivity, were measured. Data were analyzed in SPSS software (version 24) using Shapiro-Wilk, t-test correlated, and one-way analysis of variance test to investigate intra-group and inter-group effects, respectively. Results: Aerobic and resistance training causes significant changes in fat percentage, fasting blood sugar, cholesterol, triglyceride, HDL, and LDL in obese men with type 2 diabetes (P≤0/05). Moreover, in the between-group comparison, aerobic exercise causes significant changes in mean blood pressure, insulin, Insulin resistance index (HOMA-IR), adropin, and spexin levels in obese men with type 2 diabetes (P≤0/05). Conclusion: Participation in an aerobic exercise program with moderate intensity exerts more marked effects on adropin and spexin indices compared to resistance exercise. It is recommended to consider aerobic training programs in diabetic people as an effective factor in therapeutic intervention.

There are many studies on nesfatin-1, omentin, adropin, leptin, and ghrelin. However, data on the effects of long, medium, and short chain fatty acids on serum/tissue concentrations of nesfatin-1, omentin, adropin, leptin, and ghrelin are scarce. This study aims to investigate the effects of butyric acid, caprylic acid, and oleic acid alone or in combination on nesfatin-1, omentin, adropin, leptin, and ghrelin secretion. In the study, 49 male Wistar rats were used. The rats were randomly divided into 7 groups as control (CONT), butyric acid (BA), caprylic acid (CA), oleic acid (OA), butyric acid+caprylic acid (BA+CA), butyric acid+oleic acid (BA+OA) and caprylic acid+oleic acid (CA+OA) groups. The rats were orally administered fatty acids for twenty-one days. At the end of the study, the levels of nesfatin-1, omentin, adropin, leptin, and ghrelin were determined by the ELISA method. When the groups were compared in terms of nesfatin-1, omentin, adropin, leptin, and ghrelin levels, the butyric acid group had higher nesfatin-1, omentin, adropin, leptin, and ghrelin levels than the other groups (p0.05). In conclusion, it was observed that butyric acid use caused an increase in serum nesfatin-1, omentin, adropin, leptin, and ghrelin levels. [Med-Science 2023; 12(4.000): 1117-23]

Diabetes mellitus affects 537 million adults around the world. Adropin is expressed in different cell types. Our aim was to investigate the cellular localization in the endocrine pancreas and its effect on modulating pancreatic endocrine hormone release in streptozotocin (STZ)-induced diabetic rats. Adropin expression in the pancreas was investigated in normal and diabetic rats using immunohistochemistry and immunoelectron microscopy. Serum levels of insulin, glucagon pancreatic polypeptide (PP), and somatostatin were measured using a Luminex® χMAP (Magpix®) analyzer. Pancreatic endocrine hormone levels in INS-1 832/3 rat insulinoma cells, as well as pancreatic tissue fragments of normal and diabetic rats treated with different concentrations of adropin (10−6, 10−9, and 10−12 M), were measured using ELISA. Adropin was colocalized with cells producing either insulin, glucagon, or PP. Adropin treatment reduced the number of glucagon-secreting alpha cells and suppressed glucagon release from the pancreas. The serum levels of GLP-1 and amylin were significantly increased after treatment with adropin. Our study indicates a potential role of adropin in modulating glucagon secretion in animal models of diabetes mellitus.

The present study aimed to investigate the association of nutrient patterns (NPs) with metabolic health status and serum levels of brain-derived neurotrophic factor (BDNF) and adropin in Iranian adults. This cross-sectional survey was performed on 527 adults aged 20–60 years in Isfahan, Iran. To evaluate dietary intake, a validated 168-item semi-quantitative food frequency questionnaire (FFQ) was used. Participants were categorized as metabolically healthy (MH) and metabolically unhealthy (MU) according to their glycemic and lipid profile, insulin resistance (IR), and inflammation status. An overnight fasting blood sample was collected from each participant and serum levels of BDNF and adropin were assessed. A total of 42.50% of participants were recognized as MU. Three NPs were recognized by factor analysis that labeled as "high animal protein" (NP1), "high vegetable" (NP2), and "high carbohydrate" (NP3) patterns. Moderate adherence to NP2 was related to a lower risk of MU (ORT2 vs. T1 = 0.38, 95% CI: 0.18–0.76). Moreover, high adherence of NP2 (T3 vs. T1) was inversely associated with hypertriglyceridemia (OR = 0.27, 95% CI: 0.11–0.65; P-trend < 0.001) and high hs-CRP values (OR = 0.29, 95% CI: 0.09–1.00; P-trend = 0.03). No significant association was observed between adherence of NP1 and NP3 with MU in crude and adjusted models. However, negative associations were found between moderate adherence to NP3 and insulin resistance (IR) (OR = 0.23, 95% CI: 0.06–0.91) as well as high adherence to NP1 and hypertension (OR = 0.23, 95% CI: 0.09–0.61; P-trend < 0.001). NPs were not associated with serum BDNF and adropin values. [ABSTRACT FROM AUTHOR]

Adropin, a multifaceted peptide, was identified as a new metabolic hormone responsible for regulating gluco-lipid homeostasis. However, its role in the testicular function is not yet understood. We aimed to investigate the localization and expression of adropin and GPR19 during different phases of postnatal development. Immunohistochemical study revealed the intense reactivity of adropin in the Leydig cells during all phases of postnatal development, while GPR19 showed intense immunoreactivity in the pachytene spermatocytes and mild immunoreactivity in Leydig cells as well as primary and secondary spermatocytes. Western blot study revealed maximum expression of GPR19 in pre-pubertal mouse testis that clearly indicates maximum responsiveness of adropin during that period. So, we hypothesized that adropin may act as an autocrine/paracrine factor that regulates pubertal changes in mouse testis. To examine the effect of adropin on pubertal onset, we gave bilateral intra-testicular doses (0.5 and 1.5 µg/testis) to pre-pubertal mice. Adropin treatment promoted testicular testosterone synthesis by increasing the expression of StAR, 3β-HSD, and 17β-HSD. Adropin also promoted germ cell survival and proliferation by upregulating the expression of PCNA and downregulating the Bax/Bcl2 ratio and Caspase 3 expression resulting in fewer TUNEL-positive cells in adropin-treated groups. FACS analysis demonstrated that adropin treatment not only increases 1C to 4C ratio but also significantly increases the 1C (spermatid) and 1C to 2C ratio which demarcates accelerated germ cell differentiation and turnover of testicular cells. In conclusion, adropin promotes steroidogenesis, germ cell survival, as well as the proliferation in the pre-pubertal mouse testis that may hasten the pubertal transition in an autocrine/paracrine manner. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to uncover if homocysteine (Hcy) adropin balance expressed by homocysteine/adropin ratio (HAR) is related to severity of disease in coronary artery disease (CAD) patients. Materials & Methods: The present cross-sectional study 50 consecutive patients with low/intermediate CAD severity and other 50 patients with severe CAD. Hcy and adropin levels were assessed using commercially available kits. Results: Patients with low/moderate severity CAD expressed significantly lower HAR. According to HAR, all patients were classified into those with low HAR (

The secreted peptide adropin is highly expressed in human brain tissues and correlates with RNA and proteomic risk indicators for dementia. Here we report that plasma adropin concentrations predict risk for cognitive decline in the Multidomain Alzheimer Preventive Trial (ClinicalTrials.gov Identifier, NCT00672685; mean age 75.8y, SD = 4.5 years, 60.2% female, n = 452). Cognitive ability was evaluated using a composite cognitive score (CCS) that assessed four domains: memory, language, executive function, and orientation. Relationships between plasma adropin concentrations and changes in CCS (∆CCS) were examined using Cox Proportional Hazards Regression, or by grouping into tertiles ranked low to high by adropin values and controlling for age, time between baseline and final visits, baseline CCS, and other risk factors (e.g., education, medication, APOE4 status). Risk of cognitive decline (defined as a ∆CCS of − 0.3 or more) decreased with increasing plasma adropin concentrations (hazard ratio = 0.873, 95% CI 0.780–0.977, P = 0.018). Between adropin tertiles, ∆CCS was significantly different (P = 0.01; estimated marginal mean ± SE for the 1st to 3rd tertile, − 0.317 ± 0.064; − 0.275 ± 0.063; − 0.042 ± 0.071; n = 133,146, and 130, respectively; P < 0.05 for 1st vs. 2nd and 3rd adropin tertiles). Normalized plasma Aß42/40 ratio and plasma neurofilament light chain, indicators of neurodegeneration, were significantly different between adropin tertile. These differences were consistent with reduced risk of cognitive decline with higher plasma adropin levels. Overall, these results suggest cognitive decline is reduced in community-dwelling older adults with higher circulating adropin levels. Further studies are needed to determine the underlying causes of the relationship and whether increasing adropin levels can delay cognitive decline. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) is a prevalent public health problem. Uric acid (UA) is increased by MetS. We investigated whether administration of UA and 10% fructose (F) would accelerate MetS formation and we also determined the effects of irisin and exercise. We used seven groups of rats. Group 1 (control); group 2 (sham); group 3 (10% F); group 4 (1% UA); group 5 (2% UA); group 6 (10% F + 1% UA); and Group 7, (10% F + 2% UA). After induction of MetS (groups 3 -7), Group 3 was divided into three subgroups: 3A, no further treatment; 3B, irisin treatment; 3C, irisin treatment + exercise. Group 4, 1% UA, which was divided into three subgroups: 4A, no further treatment; 4B, irisin treatment; 4C, Irisin treatment + exercise. Group 5, 2% UA, which was divided into three subgroups: 5A, no further treatment; 5B, irisin treatment; 5C, irisin treatment + exercise. Group 6, 10% F + 1% UA, which was divided into three subgroups: 6A, no further treatment; 6B, irisin treatment; 6C, irisin treatment + exercise. Group 7, 10% F + 2% UA, which was divided into three subgroups: 7A, no further treatment; 7B, irisin treatment; 7C, irisin treatment + exercise., İrisin was administered 10 ng/kg irisin intraperitoneally on Monday, Wednesday, Friday, Sunday each week for 1 month. The exercise animals (in addition to irisin treatment) also were run on a treadmill for 45 min on Monday, Wednesday, Friday, Sunday each week for 1 month. The rats were sacrificed and samples of liver, heart, kidney, pancreas, skeletal muscles and blood were obtained. The amounts of adropin (ADR) and betatrophin in the tissue supernatant and blood were measured using an ELISA method. Immunohistochemistry was used to detect ADR and betatrophin expression in situ in tissue samples. The duration of these experiments varied from 3 and 10 weeks. The order of development of MetS was: group 7, 3 weeks; group 6, 4 weeks; group 5, 6 weeks; group 4, 7 weeks; group 3, 10 weeks. Kidney, liver, heart, pancreas and skeletal muscle tissues are sources of adropin and betatrophin. In these tissues and in the circulation, adropin was decreased significantly, while betatrophin was increased significantly due to MetS; irisin + exercise reversed this situation. We found that the best method for creating a MetS model was F + UA2 supplementation. Our method is rapid and simple. Irisin + exercise was best for preventing MetS. [ABSTRACT FROM AUTHOR]

Objective: There is escalating evidence suggesting the beneficial effects of ellagic acid (EA) on the cardiovascular system. The aim of the present study was to investigate the protective effect of EA in human umbilical vein endothelial cells (HUVECs) against high glucose (HG)- induced endothelial dysfunction and to study the potential roles of adropin and nitric oxide (NO) in this regard. Materials and Methods: The experimental groups consisted of normal and HG (30 mM, 48 hr)-treated HUVECs incubated without or with 5 or 10 µM of EA (6 groups of at least 6 replicates, each). The cell count and viability were studied. Moreover, the markers of the redox state, including malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and catalase enzymes, and ferric reducing anti-oxidant power (FRAP), were assayed. The levels of adropin and eNOS gene expression were also studied using RT-qPCR. Results: A high concentration of glucose reduced cell count and caused lipid peroxidation, reduced anti-oxidant capacity of the cells, decreased NO levels, and downregulated the expression of NOS3 (encoding eNOS) and ENHO (encoding adropin) genes. Ellagic acid reversed all these effects. Conclusion: These results suggest a significant protective effect for EA against HG-induced injury in HUVECs. The improved redox state and upregulation of NOS3 and ENHO genes seem to play critical roles in this regard. [ABSTRACT FROM AUTHOR]

Adropin is a versatile peptide which was discovered as a novel metabolic hormone that is involved in the regulation of lipid and glucose homeostasis. However, its possible role in the testicular function is not yet understood. The aim of our study was to explore the distribution pattern of adropin and GPR19 in various cell types and its possible role in testicular functions of adult mice. Immunohistochemical study revealed the intense immunoreactivity of adropin in the Leydig cells, while GPR19 showed intense immunoreactivity in the pachytene spermatocytes and mild immunoreactivity in Leydig cells and primary as well as secondary spermatocytes in mouse testis. Enho mRNA was also found to be expressed in the mouse testis. These findings suggested that adropin‐GPR19 signaling may act in autocrine/paracrine manner to modulate testicular functions. Furthermore, to find out the direct role of adropin in the testicular function, in vitro study was performed in which testicular slices were cultured with adropin alone (10 and 100 ng/mL) and in combination with insulin (5 μg/mL). Adropin alone inhibited testicular testosterone synthesis by inhibiting the expression of P450‐SCC, 3β‐HSD, and 17β‐HSD while along with insulin stimulated the testicular testosterone synthesis by increasing the expression of GPR19, IR, StAR, P450‐SCC, 3β‐HSD, and 17β‐HSD. Adropin alone or in combination with insulin promoted germ cell survival and proliferation by upregulating the expression of PCNA, Bcl2, and pERK1/2. Thus, it can be concluded that adropin‐GPR19 signaling promotes insulin stimulated steroidogenesis and germ cell survival as well as proliferation in the mice testes in an autocrine/paracrine manner. Research Highlights: Adropin is mainly localized in Leydig cells of the testis.GPR19 is localized in Leydig cells as well as advanced germ cells.Adropin alone inhibits steroidogenesis but promotes insulin stimulated steroidogenesis.Adropin alone or along with insulin promotes germ cell survival and proliferation. [ABSTRACT FROM AUTHOR]

Introduction: Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have a favorable impact on the kidney function in patients with heart failure (HF), while there is no clear evidence of what factors predict this effect. The aim of the study was to identify plausible predictors for kidney function outcome among patients with HF and investigate their association with SGLT2i. Methods: We prospectively enrolled 480 patients with type 2 diabetes mellitus (T2DM) treated with diet and metformin and concomitant chronic HF and followed them for 52 weeks. In the study, we determined kidney outcome as a composite of ≥ 40% reduced estimated glomerular filtration rate from baseline, newly diagnosed end-stage kidney disease or kidney replacement therapy. The relevant medical information and measurement of the biomarkers (N-terminal natriuretic pro-peptide, irisin, apelin, adropin, C-reactive protein, tumor necrosis factor-alpha) were collected at baseline and at the end of the study. Results: The composite kidney outcome was detected in 88 (18.3%) patients of the entire population. All patients received guideline-recommended optimal therapy, which was adjusted to phenotype/severity of HF, cardiovascular risk and comorbidity profiles, and fasting glycemia. Levels of irisin, adropin and apelin significantly increased in patients without clinical endpoint, whereas in those with composite endpoint the biomarker levels exhibited a decrease with borderline statistical significance (p = 0.05). We noticed that irisin ≤ 4.50 ng/ml at baseline and a ≤ 15% increase in irisin serum levels added more valuable predictive information than the reference variable. However, the combination of irisin ≤ 4.50 ng/ml at baseline and ≤ 15% increase in irisin serum levels (area under curve = 0.91; 95% confidence interval = 0.87–0.95) improved the discriminative value of each biomarker alone. Conclusion: We suggest that low levels of irisin and its inadequate increase during administration of SGLT2i are promising predictors for unfavorable kidney outcome among patients with T2DM and concomitant HF. [ABSTRACT FROM AUTHOR]

There are many studies on nesfatin-1, omentin, adropin, leptin, and ghrelin. However, data on the effects of long, medium, and short chain fatty acids on serum/tissue concentrations of nesfatin-1, omentin, adropin, leptin, and ghrelin are scarce. This study aims to investigate the effects of butyric acid, caprylic acid, and oleic acid alone or in combination on nesfatin-1, omentin, adropin, leptin, and ghrelin secretion. In the study, 49 male Wistar rats were used. The rats were randomly divided into 7 groups as control (CONT), butyric acid (BA), caprylic acid (CA), oleic acid (OA), butyric acid+caprylic acid (BA+CA), butyric acid+oleic acid (BA+OA) and caprylic acid+oleic acid (CA+OA) groups. The rats were orally administered fatty acids for twenty-one days. At the end of the study, the levels of nesfatin-1, omentin, adropin, leptin, and ghrelin were determined by the ELISA method. When the groups were compared in terms of nesfatin-1, omentin, adropin, leptin, and ghrelin levels, the butyric acid group had higher nesfatin-1, omentin, adropin, leptin, and ghrelin levels than the other groups (p<0.05). No statistically significant difference was found in the other groups (p>0.05). In conclusion, it was observed that butyric acid use caused an increase in serum nesfatin-1, omentin, adropin, leptin, and ghrelin levels. [ABSTRACT FROM AUTHOR]

BackgroundSubarachnoid hemorrhage (SAH) is a life-threatening vascular condition without satisfactory treatment options. The secreted peptide adropin is highly expressed in the human brain and has neuroprotective effects in brain injury models, including actions involving the cerebrovasculature. Here, we report an endothelial nitric oxide synthase (eNOS)-dependent effect of synthetic adropin treatment that reverses the deleterious effects of SAH.MethodsWe tested the molecular, cellular, and physiological responses of cultured brain microvascular endothelial cells and two mouse models of SAH to treatment using synthetic adropin peptide or vehicle.ResultsSAH decreases adropin expression in cultured brain microvascular endothelial cells and in murine brain tissue. In two validated mouse SAH models, synthetic adropin reduced cerebral edema, preserved tight junction protein expression, and abolished microthrombosis at 1 day post-SAH. Adropin treatment also prevented delayed cerebral vasospasm, decreased neuronal apoptosis, and reduced sensorimotor deficits at seven days post-SAH. Delaying initial treatment of adropin until 24 h post-SAH preserved the beneficial effect of adropin in preventing vasospasm and sensorimotor deficits. Mechanistically, adropin treatment increased eNOS phosphorylation (Ser1179) at 1 & 7 days post-SAH. Treating eNOS−/− mice with adropin failed to prevent vasospasm or behavioral deficits, indicating a requirement of eNOS signaling.ConclusionsAdropin is an effective treatment for SAH, reducing cerebrovascular injury in both the acute (1 day) and delayed (7 days) phases. These findings establish the potential of adropin or adropin mimetics to improve outcomes following subarachnoid hemorrhage.

Background and Aim: Diabetes is a metabolic disorder characterized by an elevated blood glucose level, resulting from impairments in insulin action, insulin secretion, or both; which causes abnormalities in the metabolism of carbohydrates, protein, and lipids. Chronic hyperglycemia is associated with long-term damage, dysfunction, and failure of various organs. Adropin and irisin are newly described proteins that can be an essential component in the pathophysiological pathways of diabetes mellitus. The current study was designed to evaluate Irisin and Adropin biochemical markers in patients with type 2 diabetes mellitus and their correlation with risk factors. Materials and Methods: A case control study, that included 90 patients of type 2 diabetes mellitus and 90 healthy individuals, who matched for both age and sex with patients. Fasting blood sugar (FBS), HbA1c, serum insulin, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG), irisin and adropin were measured at the chemistry laboratory of AL-Faihaa teaching Hospital by standard methods. Results: Serum irisin (8.154±1.642 vs. 14.06±3.916 ng/ml) and adropin (25.39±8.897 vs. 59.43±8.768 pg/ml) levels were significantly lower in the patient group than in the control cases, respectively (P.value

Abstract Adropin is encoded by the energy homeostasis-associated (ENHO) gene and widely present in liver, pancreas, heart, kidney, brain, and vascular tissues. Abnormal adropin is associated with metabolic, inflammatory, immune, and central nervous disorders. Whether adropin is involved in the development of colorectal cancer (CRC) is still unclear. Here, decreased adropin expression of tumor-nest cells in advanced-stage CRC was demonstrated. Adropin expressed by carcinoma cells was negatively correlated with macrophage infiltration in the matrix of CRC tissues. However, tumor macrophages enhanced adropin expression and were positively correlated with tumor invasion and metastasis. ENHO gene transfection into colon cancer (MC38) cells inhibited tumor growth in vivo, accompanying the increase of M1 macrophages. Treatment with low-dose adropin (

Aim:Stroke should be diagnosed quickly and accurately in emergency settings. This study investigated serum adropin levels as a novel biomarker in the diagnostic value of ischemic stroke.Materials and Methods:A prospective cross-sectional study was conducted in a tertiary university hospital. Serum adropin levels were measured at the time of the first arrival in ischemic stroke patients (n=46) and healthy control (n=45). In the ischemic stroke group, blood samples were retaken 72 h after arrival.Results:There was a significant difference between the ischemic stroke group and the control group regarding adropin values at arrival (2.67+0.63 vs. 2.34+0.69, respectively p=0.032). There was no significant difference between the other groups in terms of arrival values (p>0.05). Logistic regression analysis revealed a statistically significant difference between the ischemic stroke and control groups (odds ratio: 2.23; 95% confidence interval: 1.140-4.360, p=0.019). In the ischemic stroke group, the adropin level was statistically significantly decreased on the third day compared with the arrival (p=0.041). The adropin levels predicted ischemic stroke patients with 58.7% sensitivity and 59.4% specificity with the 2.49 ng/mL cut-off value (area under the curve=0.635).Conclusion:In this study, high serum adropin levels can be thought to be supportive in the diagnostic value of ischemic stroke.

Adropin—a multifunctional peptide with tissue-protective capacity that regulates energy homeostasis, sensitivity to insulin and inflammatory response—seems to show an inverse association with the presence of cardiovascular and renal diseases, obesity and diabetes mellitus in the general population. The purpose of the study is to elucidate whether adropin may be a plausible predictive biomarker for clinical outcomes in post-ST elevation of myocardial infarction (STEMI) patients with newly diagnosed prediabetes according to the American Diabetes Association criteria. A total of 1214 post-STEMI patients who received percutaneous coronary intervention were identified in a local database of the private hospital “Vita Center” (Zaporozhye, Ukraine). Between November 2020 and June 2024, we prospectively enrolled 498 patients with prediabetes in this open prospective cohort study and followed them for 3 years. The combined clinical endpoint at follow-up was defined as cardiovascular death due to acute myocardial infarction, heart failure, sudden death due to arrhythmia or cardiac surgery, and/or all-cause death. We identified 126 clinical events and found that serum levels of adropin < 2.15 ng/mL (area under the curve = 0.836; 95% confidence interval = 0.745–0.928; sensitivity = 84.9%; specificity = 72.7%; likelihood ratio = 3.11; p = 0.0001) predicted clinical outcomes. Multivariate logistic regression showed that a Gensini score ≥ 32 (Odds ratio [OR] = 1.07; p = 0.001), adropin ≤ 2.15 ng/mL (OR = 1.18; p = 0.001), use of SGLT2i (OR = 0.94; p = 0.010) and GLP-1 receptor agonist (OR = 0.95; p = 0.040) were independent predictors of clinical outcome. Kaplan–Meier plots showed that patients with lower adropin levels (≤2.15 ng/mL) had worse clinical outcomes compared to patients with higher adropin levels (>2.15 ng/mL). In conclusion, low levels of adropin (≤2.15 ng/mL) independently predicted clinical outcomes in post-STEMI patients with newly detected prediabetes and improved the discriminative ability of the Gensini score for 3-year follow-up events. Future clinical studies are needed to clarify whether adropin is a promising molecule to be incorporated into conventional risk scores for the prediction of MACCEs after STEMI.

In patients with type 2 diabetes mellitus (T2DM), asymptomatic adverse cardiac remodeling plays a pivotal role in the development of heart failure (HF). Patients with T2DM often have low or near-normal levels of natriuretic peptides, including N-terminal brain natriuretic peptide (NT-proBNP), which have been inconclusive in predicting the transition from asymptomatic adverse cardiac remodeling to HF with preserved ejection fraction (HFpEF). The aim of this study was to elucidate the predictive ability of adropin for HFpEF depending on the circulating levels of NT-proBNP. We prospectively enrolled 561 T2DM patients (glycated hemoglobin < 6.9%) with echocardiographic evidence of structural cardiac abnormalities and left ventricular ejection fractions >50%. All patients underwent B-mode transthoracic echocardiographic and Doppler examinations. Circulating biomarkers, i.e., NT-proBNP and adropin, were assessed at baseline. All individuals were divided into two groups according to the presence of low levels (n = 162) or elevated levels (≥125 pmol/mL; n = 399) of NT-proBNP. Patients with known asymptomatic adverse cardiac remodeling and elevated NT-proBNP were classified as having asymptomatic HFpEF. A multivariate logistic regression showed that low serum levels of adropin (