Adropin Levels Research Articles

P050 Serum adropin levels in patients with Crohn’s disease

P050 Serum adropin levels in patients with Crohn’s disease

Serum adropin levels in psoriasis vulgaris and its relation with metabolic parameters

Background/aim Adropin is a peptide-structure hormone that plays a role in preventing the development of insulin resistance, which has been linked to obesity and metabolic regulation. The purpose of this study is to assess serum adropin levels and their relationship with metabolic parameters in psoriasis vulgaris patients both with and without metabolic syndrome (MetS).Materials and methods Fifty-three patients and 26 healthy controls were included in this study. Serum adropin levels, fasting blood glucose, fasting serum insulin, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, and triglyceride levels of all participants were analyzed. Enzyme-linked immunosorbent assay was used to measure serum adropin levels. Results Serum adropin levels were 2.94 ± 0.56 ng/mL in psoriatic patients without MetS, 2.49 ± 0.77 ng/mL in psoriasis patients with MetS, and 3.37 ± 0.71 ng/mL in the control group. Multivariate logistic regression analysis was used to evaluate adropin decreases in psoriasis patients as an independent predictor of the presence of MetS. Conclusion The serum levels of adropin in psoriasis patients were significantly lower in the presence of MetS, and this decrease was more prominent than in those without MetS. Adropin may be a contributing factor for metabolic disorders and the development of MetS in psoriasis patients.

Serum Adropin Levels Are Reduced in Adult Patients with Nonalcoholic Fatty Liver Disease

Objectives: Adropin is a novel marker of metabolic syndrome and insulin resistance. The aim of this study was to explore the association of serum adropin levels with hepatosteatosis among adult patients. Materials and Methods: Serum biochemical parameters including liver and renal function tests, insulin levels, and serum adropin levels were compared between adult patients with nonalcoholic fatty liver disease (NAFLD) and healthy control cases. Results: A total of 51 patients with a mean age of 37.9 ± 9.96 years diagnosed with grade 2–3 hepatosteatosis and 30 healthy control cases with a mean age of 34.8 ± 9.5 years were included in the study. Serum adropin levels in the NAFLD group were statistically significantly lower than in the control cases (588.4 ± 261.0 vs. 894.2 ± 301.2, respectively; p < 0.001). The study participants were further subdivided into 2 groups as patients with (n = 35) or without (n = 46) insulin resistance using the serum homeostatic model of assessment-insulin resistance (HOMA-IR). Serum adropin levels were statistically significantly lower in patients with insulin resistance (p < 0.01). There was a negative correlation between adropin levels and serum insulin, HOMA-IR, urea, gamma-glutamyl transferase, total cholesterol, and triglyceride levels. Conclusion: We observed a decrease in serum adropin levels among adult patients with NAFLD. We also found lower levels of serum adropin in patients with insulin resistance, supporting previous data in the literature. Studies investigating the association of adropin levels with other inflammatory parameters are warranted to define its exact role in the pathogenesis of hepatosteatosis.

Serum adropin levels in patients with acute ischemic stroke

Stroke is one of the principal diseases leading to death and permanent disability worldwide. One of the main causes of stroke is atherosclerosis. A decrease in Adropin levels has been identified as an independent predictor of atherosclerosis development. The purpose of this study was to determine serum Adropin levels in patients with acute ischemic stroke (AIS) and to investigate the relation between Adropin levels and stroke. Fifty-nine patients presenting to the emergency department with symptoms of stroke and diagnosed with AIS, and 51 healthy individuals representing the control group, were included in the study. Patient and control group demographic data and clinical characteristics were recorded. Serum Adropin levels were studied in blood specimens collected from both groups. The results were then compared. Patient group serum Adropin levels were significantly lower than those of the control group (2.16±0.76, and 2.72±1.01, respectively p=0.002). Multivariate logistic regression analysis identified a low serum Adropin level as an independent predictor of stroke (OR=0.420, 95% Cl=0.221-0.801, p=0.008). We also determined significant inverse correlation between serum Adropin levels and glucose levels (r= -0.345, p=0.013). Our study suggested that, low serum Adropin levels are associated with AIS. Adropin may be used as a screening tool for AIS.

Effects of Vitamin D on adropine and apoptosis in kidney tissue

Aim: This study aims to investigate the effects of vitamin D on adropin and apoptosis in rat kidney tissue in the context of the experimental diabetes model created using streptozotocin (STZ).Material and Methods: 41 male Wistar-albino breed rats of 8-10 weeks were distributed into 5 groups, which consisted of 3 groups with 7 animals each and 2 groups with 10 animals each. No treatments were applied to the control group. The Buffer group was administered with single-dose 0.1 M sodium buffer intraperitoneally (ip). The Vitamin D group was orally administered 200 IU/day vitamin D. The Diabetes group was injected ip with single-dose 50 mg/kg STZ by dissolving the material in 0.1 M sodium buffer.Results: The biochemical and histological investigations revealed similar serum TOS and TAS levels, and TUNEL positivity and Adropin immunoreactivity for the Control, Buffer, and Vitamin D groups. While TOS levels and TUNEL positivity were significantly higher in the Diabetes group compared to the Control group, TAS levels and Adropin immunoreactivity were significantly lower. The TOS levels and TUNEL positivity were significantly reduced in the Diabetes+Vitamin D group compared to the diabetic group, and TAS levels, adropin immunoreactivity were significantly higher. Conclusion: In conclusion; it was determined that experimental diabetes increased TOS and apoptotic cells and decreased TAS and adropin levels in the kidney tissue in experimental diabetes, and that Vitamin D administered as treatment decreased TOS and apoptotic cells and increased TAS and Adropin levels. It was concluded that in order to uncover the role of diabetes in the pathophysiology of its effect on kidney tissue, future studies that consider various experimental diabetes times were necessary.

Serum adropin as a predictive biomarker of erectile dysfunction in coronary artery disease patients.

IntroductionErectile dysfunction (ED) is associated with various comorbidities and an early diagnosis and treatment is necessary to avoid the development of these comorbidities. Unfortunately, there is no biochemical marker that can be used for early diagnosis of ED. Nitric oxide (NO) is released by nerve and endothelial cells in the corpora cavernosa of the penis and is believed to be the main vasoactive chemical mediator of penile erection. Adropin is a regulatory peptide which has effects on NO bioavailability and energy homeostasis. We hypothesized that adropin may contribute to the pathogenesis of ED because of the presence of both metabolic effects and the influence on NO bioavailability. To confirm this hypothesis, we investigated the relationship between ED and serum adropin and NO levels.Material and methodsSeventy-five ED patients were enrolled for this study and the patients were divided into two groups according to angiographic scoring. Serum NO and adropin levels were measured by the Griess reaction and ELISA method, respectively.ResultsSerum adropin and NO levels were found to be lower in the group which has higher angiographic score and the difference in NO was statistically significant. Also, adropin has a significant correlation between IIEF scores in ED patients.ConclusionsThis is the first study in the literature investigating the levels of adropin in ED patients having coronary artery disease. The adropin molecule shows a promising future in clarifying the etiopathogenesis of ED. More comprehensive and multicenter studies are needed to reveal the role of adropin in ED and the effects of treatment on this molecule.

Plasma Adropin as a Potential Marker Predicting Obesity and Obesity-associated Cancer in Korean Patients With Type 2 Diabetes Mellitus.

BackgroundType 2 diabetes mellitus (T2DM) and cancer are serious health problems worldwide, and their prevalences have been on the rise in recent years. It has been reported that adropin plays an important role in the development of T2DM, oxidative stress, inflammation, and obesity. However, there is limited information available on T2DM from human studies, especially for the Korean population. In this study, we aimed to investigate the correlation between adropin levels and obesity of Korean T2DM patients.MethodsThirty-six T2DM patients were recruited for this study. The participants were further classified into female (n = 12) and male (n = 24). Their body composition, metabolic parameters, inflammatory factors, and oxidative stress were measured.ResultsThe severity of obesity is more manifested in male than in female. Plasma triglyceride (TG) and high-sensitivity C-reactive protein (hs-CRP) levels of male were significantly higher than female. The plasma adropin and adiponectin level of female was significantly higher than male. The body weight, body mass index (BMI), body fat mass were negatively correlated with the plasma adropin level in female, whereas adropin has positive correlation with adiponectin in female. The hs-CRP was negatively correlated with the plasma adropin level in female and male. malondialdehyde, reactive oxidative species, and TNF-α was not significantly correlated with adropin in patients with T2DM.ConclusionsThese findings suggest that adropin may be more used as a biomarker for predicting the risk of obesity and inflammation in Korean patients with T2DM, especially women.

Adropin protects against liver injury in nonalcoholic steatohepatitis via the Nrf2 mediated antioxidant capacity

Adropin, a secretory signal peptide, has shown beneficial effects on improving glucose homeostasis and dyslipidemia. However, whether this peptide affects nonalcoholic steatohepatitis (NASH) has remained unclear. In this study, the serum adropin levels, liver injury and oxidative stress were measured in diet-induced NASH mice. Adropin knock-out mice and palmitate treated primary hepatic cells were used to investigate the influence of adropin on liver injury. Our results show that serum adropin levels were decreased and negatively correlated with liver injury in NASH mice. Knockout of adropin significantly exacerbated hepatic steatosis, inflammatory responses and fibrosis in mice after either methionine-choline deficient diet (MCD) or western diet (WD) feeding. And the treatment with adropin bioactive peptides ameliorated NASH progression in mice. Adropin alleviated hepatocyte injury by upregulating the expression of Gclc, Gclm, and Gpx1 in a manner dependent on Nrf2 transcriptional activity and by increasing the glutathione (GSH) levels. And adropin significantly increased CBP expression and promoted its binding with Nrf2, which enhanced Nrf2 transcriptional activity. Furthermore, AAV8-mediated overexpression of hepatic Nrf2 expression functionally restored the liver injury induced by adropin-deficiency MCD-fed mice. These findings provide evidence that adropin activates Nrf2 signaling and plays a protective role in liver injury of NASH and therefore might represent a novel target for the prevention and treatment of NASH.

Serum Adropin Levels in a Preeclampsia Like L-Name Rat Model Treated with Sildenafil Citrate

AbstractBackground: Preeclampsia, a hypertensive disorder of pregnancy, is detrimental to both mother and fetus. Sildenafil been proposed as a potential therapy to reduce blood pressure and improve uteroplacental perfusion in preeclamptic patients. Adropin is a novel secreted energy homeostasis protein regulating carbohydrate, lipid and protein metabolism, maternal adropin levels in Preeclampsia were still controversy.Aim of the Work: To evaluate serum levels of adropin in preeclampsia-like rat model and in preeclamptic rats treated with Sildenafil and to investigate their associations with some inflammatory, oxidative stress, and metabolic parameters.Material and Methods: 32 pregnant rats were divided randomly into four groups (n=8): Control group, sildenafil treated group, L-NAME group to induce pre-eclampsia and L-NAME with sildenafil treated group. In all groups, maternal Body Mass Index (BMI), placental weights, fetal weights, maternal mean arterial blood pressure (MAP), total urinary proteins, serum glucose, insulin and calculated Homeostatic Model Assessment of Insulin Resistance index (HOMA-IR), serum urea, creatinine, Triglycerides (TGs), Total Cholesterol (TC), Low Density Lipoproteins-cholesterol (LDL-c), High Density Lipoproteins-cholesterol (HDL-c), C Reactive Protein (CRP), Endothelin-1 (ET-1), and adropin were measured, also placental Malondialdehyde (MDA) levels, and activities of the antioxidant enzymes Superoxide Dismutase (SOD) and glutathione peroxidase (GSH) in placental homogenates were determined plus histopathological examination of placental sections were done.Results: L-NAME induced preeclampsia in rats and they showed significant increase in MAP, total urinary proteins, serum levels of glucose, insulin, calculated HOMA-IR, serum urea, creatinine, CRP, ET-1, TGs, TC, LDL-c, adropin and placental tissue MDA with significant reduction in maternal BMI, placental weights, fetal weights, serum HDL-c and placental tissue SOD and GSH activities as compared to other groups, additionally, L-NAME treated and L-NAME + SILD treated groups revealed positive significant correlations between adropin levels and MAP, total urinary proteins, serum levels of urea, creatinine, CRP, ET-1, TGs, TC, LDL-c, and placental tissue MDA, however they showed negative corre-lations between adropin and BMI, placental weights, fetal weights, serum HDL-c and placental tissue SOD and GSH activities.Conclusion: Increased maternal adropin levels in preec-lampsia like model in rats might represent a regulatory feed-back mechanism against endothelial placental dysfunction, insulin resistance, inflammation and oxidative stress which associated with preeclampsia, hence identify it as a potentially protective agent against preeclampsia development. Sildenafil ameliorates preeclampsia symptoms, inflammation and oxi-dative stress in a rat model of preeclampsia.

Relationship of Adropin Level and Inducible Nitric Oxide Synthase with the Phases of Intestinal Ischemia-Reperfusion in Rats

AbstractBackground: Adropin is a peptide hormone that plays an important role in energy homeostasis and endothelial functions. Nitric oxide is a potent vasodilator synthesized in the vascular endothelium from the Nitric Oxide Synthase enzyme (NOS). There are controversial studies about the role of NOS and its isoforms the endothelial (eNOS) and the inducible (iNOS) forms in Ischemia-Reperfusion (IR) injury. It was found that adropin influences gene expression of eNOS and enhances endothelial cell function. However, few researchers have studied the link between adropin and iNOS activity during different phases of IR-injury.Aim of the Study: To estimate the plasma level of adropin, and iNOS activity and to study the relationship of both of them and their role during different phases of intestinal IR-injury in rats.Material and Methods: A total of 20 rats were used in this study (200-220g). Rats were divided into two groups (10 rats/each); group I (sham-operated group) and group II which exposed to laparotomy and occlusion of the superior mesenteric artery for 30min the reperfusion for 60min. Serial blood samples were taken via an inserted carotid catheter at 0, 30, and 90min. Plasma levels of adropin and iNOS were measured by ELISA kits according to the manufacturer protocols. The contents of the intestinal lumen were centrifuged and examined for detection of hemoglobin and albumin concentrations. ANOVA with a post hoc test, independent sample t-test, and Person correlation were used for statistical analyses.Results: Plasma adropin level and iNOS activity are significantly increased during ischemic and reperfusion phases of intestinal IR-injury when compared to the pre-ischemic phase of group II or when compared to the sham-operated group. Adropin was significantly correlated with iNOS during all phases. Moreover, unlike adropin, the iNOS level was correlated with the severity of the intestinal bleeding.Conclusion: Plasma adropin level is positively correlated with iNOS activity during different phases of intestinal IR-injury in rats, and this may provide new markers for diagnosis of IR-injury during intestinal surgeries.

Effect of Metformin Pretreatment on Serum Adropin Level in Rats with Adrenalin-Induced Acute Myocardial Infarction

AbstractBackground: Beside adropin's role in energy homeostasis and insulin sensitivity, it is also incriminated in myocardial ischemia. Level of adropin during myocardial infarction (MI) and the effect of metformin pretreatment on serum adropin level in rat models of MI is underinvestigated.Aim of Study: This study investigated the level of adropin in MI and the possible involvement of adropin and endothelial nitric oxide synthase enzyme activity (eNOS) in the cardio-protective effect of metformin during acute myocardial ischemia.Material and Methods: A total of forty adult male albino rats weighing 185-220g were divided equally into four groups Group I: Normal control group. Group II: MI group, which was induced by subcutaneous injection of adrenalin (2mg/kg) in two doses 24 hours apart. Group III: Normal rats which were treated with oral metformin via a feeding tube in a dose of 300mg/kg for 2 weeks. Group IV: Rats with adrenalin-induced MI and pretreated with oral metformin in the same dose and duration before induction of MI on the 13th and 14th days of the study. Serum adropin and eNOS were measured, in addition to cardiac troponin I, Creatine Kinase isoenzyme (CK-MB), and C-reactive protein (CRP). Sections from the heart was stained with Masson's trichrome stain and examined to quantify the degree of ischemic injury at the tissue level.Results: In MI group, both serum adropin level and the eNOS were significantly increased with significant positive correlation between adropin and troponin I, CK-MB, and eNOS in the same group (r= 0.857, 0.97 & 0.845, respectively, p<0.05). However, Metformin pretreatment in group IV, produced significant reduction in the level of adropin accom-panied by significant increase in levels of eNOS enzyme activity in comparison to rats with untreated MI. Additionally histological examination, showed reduction of the inflamma-tory cell infiltration, myocardial fibrosis and necrosis. More-over, there was a positive correlation between adropin and eNOS in the same group (r=0.682, p<0.05).Conclusion: Adropin and eNOS enzyme play a vital role in the pathophysiology of acute myocardial infarction. In addition, the cardioprotective effect of metformin pretreatment in this condition depends on enhancing the activity of eNOS enzyme independent on adropin level.

AEROBIC EXERCISE AND AMELIORATED ENDOTHELIAL FUNCTION IN EXPERIMENTAL PREECLAMPSIA IN RAT MODEL p

Background: Preeclampsia is a life threatening state. Aerobic exercise has a beneficial effect on vascular endothelium function. Adropin is a newly discovered peptide that can increase by exercise and decreased in endothelial dysfunction. Objectives: Detecting the effect of practicing exercise on preeclampsia pathophysiology, and role of adropin. Patients and Methods: Twenty four adult female albino wistar rats were divided into 3 equal groups: group I: Sham-operated Time-mated pregnant rats (Sham), group II: Reduced uterine perfusion pressure pregnant rats (RUPP); placental ischemia was induced at gestation day (GD) 14 to mimic preeclampsia, and group III: exercise treated reduced uterine perfusion pressure pregnant rats (Ex-RUPP); swimming started from GD1 till the end of pregnancy period, 1h/day, 6 days/week added to preeclampsia induction. Maternal arterial blood pressure, micro-albuminuria, serum urea, creatinine and calculated glomerular filtration rate (GFR), plasma insulin, glucose and calculated HOMA-IR and placental eNOS, adropin, soluble fms–like tyrosine kinase 1 (sFlt-1), malondialdehyde (MDA), total antioxidant capacity (TAC), and TNF-α were measured. Placental and fetal tissues were weighed and placenta was histo-pathologically assessed. Results: Aerobic exercise during pregnancy caused significant reductions in all blood pressure values at GD17 and 19, serum urea, creatinine, micro-albuminuria, placental anti-angiogenic sflt-1, MDA, TNF-α, plasma glucose, insulin and HOMA-IR. In addition, exercise significantly increased the calculated creatinine clearance, placental eNOS and placental adropin, placental weight, fetal weight and number. Apoptotic trophoblasts and neutrophil aggregates were absent. Adropin was significantly positive correlated with eNOS together with a significant negative correlation to mean arterial blood pressure at GD19, sflt-1, MDA, insulin and HOMA-IR. Conclusion: Aerobic exercise, through increasing adropin level, was able to restore the angiogenic balance, and to decrease the oxidative stress, and inflammatory and insulin resistance states, thus improving endothelial function. This was reflected in improvement in the renal functions, blood pressure reduction with better maternal and fetal outcome.

ENHO gene expression and serum adropin level in rheumatoid arthritis and systemic lupus erythematosus.

Adropin, a secreted protein, is encoded by the energy homeostasis-associated gene (ENHO). It is expressed by a variety of tissues and cells. It has been implicated in several physiological and pathological processes, such as angiogenesis and apoptosis. The aim of the present study was to investigate the ENHO gene expression and serum adropin levels in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The study included 36 patients with RA, 22 patients with SLE and 20 healthy controls (HC). Patients with a disease activity score-28-erythrocyte sedimentation rate (DAS28-ESR) >2.6 in the RA group and an SLE disease activity index (SLEDAI) >6 in the SLE group were accepted as active. Serum adropin levels were analyzed by the enzyme-linked immunosorbent assay (ELISA) method. The ENHO gene and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) gene expressions in peripheral blood mononuclear cells were analyzed by real-time polymerase chain reaction (PCR). The ENHO gene mRNA expression was significantly higher in the RA group than in the HC group (p = 0.024), although it was similar between the SLE and HC groups (p = 0.920). On the other hand, there were no significant differences among the study groups in terms of serum adropin levels (p > 0.05 for all). Moreover, there was no significant difference in terms of the ENHO expression and serum adropin levels between active and inactive RA and SLE patients. Although the ENHO gene expression is increased, serum adropin level is not altered in RA. Similarly, adropin seems not to be associated with SLE. However, the potential link between adropin and inflammatory diseases need to be tested by further studies.

Adropin and Inflammation Biomarker Levels in Male Patients With Obstructive Sleep Apnea: A Link With Glucose Metabolism and Sleep Parameters.

The main objectives of the study were to determine plasma adropin, systemic inflammation biomarker levels, and glucose metabolism parameters in patients with moderate and severe obstructive sleep apnea (OSA) compared to healthy controls. In this study, we included 50 male patients with OSA (25 moderate and 25 severe) and 25 age- and sex-matched control subjects. All subjects underwent fasting sampling of peripheral blood for laboratory analyses. Adropin plasma levels were significantly lower in the severe OSA group in comparison with the moderate and control groups (4.50 ± 1.45 versus 6.55 ± 1.68 versus 8.15 ± 1.79 ng/mL, P < .001). Plasma biomarkers of systemic inflammation were significantly increased in patients with moderate OSA (interleukin [IL]-6 and tumor necrosis factor alpha [TNF-α]) and severe OSA (IL-6, TNF-α, high-sensitivity C-reactive protein) when compared with controls (P < .001). Adropin levels showed a significant negative correlation with IL-6 (r = -.419, P < .001), TNF-α (r = -.540, P < .001), fasting glucose (r = -.331, P = .004), hemoglobin A1c (r = -.438, P < .001), homeostatic model assessment insulin resistance index (r = -.213, P = .046), and polysomnographic parameters including apnea-hypopnea index (r = -.615, P < .001) and oxygen desaturation index (r = -.573, P < .001). A multivariate regression analysis showed that plasma adropin remained as a significant negative predictor of severe OSA status, when adjusted for age and body mass index and computed along with other inflammatory biomarkers in the regression model (odds ratio 0.069, 95% confidence interval 0.009-0.517, P = .009). Plasma adropin concentrations significantly correlate with indices of disease severity in patients with OSA, suggesting that adropin potentially plays an important role in the complex pathophysiology of the disease.

Low Serum Adropin Levels are Associated with Coronary Slow Flow Phenomenon.

Adropin is a peptide hormone expressed in coronary artery endothelial cells, which plays a potential endothelial protective role. We sought to assess whether serum adropin levels are correlated with the coronary slow flow phenomenon (CSFP). We enrolled 82 patients with angiographically confirmed CSFP and 184 age-matched controls. Serum adropin levels were measured by enzyme-linked immunosorbent assay (ELISA), and coronary flow rate was assessed using thrombolysis in myocardial infarction (TIMI) frame count (TFC). CSFP was defined as a corrected TIMI-TFC greater than two standard deviations from the normal range. Serum adropin levels were significantly lower in the CSFP patients (n = 82) than in the controls (n = 184) (4.03 ± 1.99 vs. 4.86 ± 1.88 ng/ml, p = 0.001). Multivariate logistic regression analysis revealed that serum adropin was the only independent negative predictor of CSFP (odds ratio 0.758, 95% confidence interval 0.647-0.888, p = 0.001). Serum adropin levels were independently and negatively correlated with mean TFC (r = -0.387, p < 0.001). We demonstrated that decreased serum adropin levels were independently associated with the presence and severity of angiographically proven CSFP. These findings suggest that serum adropin may be a potential biomarker to provide valuable information regarding the prediction of CSFP.

Adropin Contributes to Anti-Atherosclerosis by Suppressing Monocyte-Endothelial Cell Adhesion and Smooth Muscle Cell Proliferation.

Adropin, a peptide hormone expressed in liver and brain, is known to improve insulin resistance and endothelial dysfunction. Serum levels of adropin are negatively associated with the severity of coronary artery disease. However, it remains unknown whether adropin could modulate atherogenesis. We assessed the effects of adropin on inflammatory molecule expression and human THP1 monocyte adhesion in human umbilical vein endothelial cells (HUVECs), foam cell formation in THP1 monocyte-derived macrophages, and the migration and proliferation of human aortic smooth muscle cells (HASMCs) in vitro and atherogenesis in Apoe−/− mice in vivo. Adropin was expressed in THP1 monocytes, their derived macrophages, HASMCs, and HUVECs. Adropin suppressed tumor necrosis factor α-induced THP1 monocyte adhesion to HUVECs, which was associated with vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 downregulation in HUVECs. Adropin shifted the phenotype to anti-inflammatory M2 rather than pro-inflammatory M1 via peroxisome proliferator-activated receptor γ upregulation during monocyte differentiation into macrophages. Adropin had no significant effects on oxidized low-density lipoprotein-induced foam cell formation in macrophages. In HASMCs, adropin suppressed the migration and proliferation without inducing apoptosis via ERK1/2 and Bax downregulation and phosphoinositide 3-kinase/Akt/Bcl2 upregulation. Chronic administration of adropin to Apoe−/− mice attenuated the development of atherosclerotic lesions in the aorta, with reduced the intra-plaque monocyte/macrophage infiltration and smooth muscle cell content. Thus, adropin could serve as a novel therapeutic target in atherosclerosis and related diseases.

The Impact of Acute Tetrahydrobiopterin Administration on Plasma Adropin Concentration in Patients with Systemic Sclerosis

BackgroundSystemic sclerosis (SSc) is an autoimmune disease characterized by inflammation, fibrosis, and profound vascular dysfunction. Adropin, a protein encoded by the Energy Homeostasis Associated gene (ENHO), has recently been shown to have direct effects on endothelial function [1], and as such, has been identified as a novel therapeutic target for treatment of vascular dysfunction. Our group has previously reported that administration of tetrahydrobiopterin (BH4) improved vascular function in SSc patients [2], ostensibly through its role as an essential endothelial nitric oxide synthase (eNOS) cofactor. However, the impact of BH4 administration on other related pathways has not been thoroughly investigated. Therefore, the aims of this study were (1) to determine if plasma adropin concentration differed between SSc patients and healthy controls, and (2) to assess the impact of acute oral BH4 administration on plasma adropin concentration in SSc patients.MethodsThirteen SSc patients (4 male, 9 female; age 60 ± 3 yrs; ht 171 ± 3 cm; wt 76 ± 4 kg) and 15 healthy controls (4 male, 11 female; age 62 ± 3 yrs; ht 163 ± 2 cm; wt 62 ± 3 kg) participated in this study. Venous blood samples were taken following a 5 hour fast. SSc patients consumed either BH4 (10 mg/kg) or placebo in randomized order 5 hours prior to arrival at the laboratory. Plasma adropin concentration was assessed by means of an enzyme‐linked immunosorbent assay kit (ELISA; Phoenix Pharmaceuticals, Inc., Burlingame, CA).ResultsPlasma adropin concentration was significantly lower in SSc patients compared to healthy, age‐matched controls (1.98 ± 0.02 vs. 2.07 ± 0.03 ng/mL, p=0.02). In SSc patients, plasma adropin concentration increased following acute BH4 administration (1.98 ± 0.02 to 2.00 ± 0.01 ng/mL, placebo vs. BH4, p=0.05), a restoration that neared values observed in the control group (p=0.06, SSc BH4 vs. control).ConclusionsSSc patients demonstrate a disease‐related reduction in plasma adropin concentration that can be increased by acute BH4 administration, rescuing adropin levels to near that of healthy controls. Together, these findings suggest that adropin may represent a novel therapeutic target in SSc, though further investigation is needed to explore the mechanisms by which BH4 may alter this pathway and subsequently impact endothelial function.Support or Funding InformationFunding: This project is funded in part by the National Institutes of Health (HL118313) and the U.S. Department of Veterans Affairs (RX001697, RX001418, E6910R).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

A novel biomarker in patients with knee osteoarthritis: adropin.

Adropin is newly discovered peptide hormone. Osteoarthritis (OA) is a kind of joint disease characterized by progressive joint cartilage loss and joint pain. The present study was carried out to investigate adropin and tumor necrosis factor alpha (TNF-α) levels and the relationship between adropin in patients with knee OA classified by Kellgren-Lawrence (KL). A total of 60 knee OA patients and 30 healthy controls were included in this study. KL grading was carried out using the radiographic findings. Demographic characteristics and laboratory parameters were recorded. Adropin and TNF-α levels were determined by using enzyme-linked immunosorbent assay (ELISA). Adropin level was lower in the knee OA patients compared with the healthy controls (p < 0.001), whereas TNF-α level was higher (p < 0.001). Adropin level was negatively correlated with TNF-α level, blood white blood cell (WBC) count, and neutrophil-lymphocyte ratio (NLR). However, there was a significant decrease in adropin level and an increase in TNF-α level parallel to the increase in the KL grade. In addition, serum adropin level was found to be significantly lower in KL grade 1 groups compared with healthy controls (p < 0.01). There was a decrease in adropin level parallel to the increase in the body mass index (BMI), and there was a statistically significant decrease in adropin level in knee OA patients higher than BMI > 30 (p < 0.01). Mean NLR of KL grade 4 was significantly increased compared with other grades (p < 0.05). The consequence of the present study suggested that serum adropin level could be used as a new biomarker indicating the early grade of knee OA.

Adhesive Capsulitis and Its Predictors in Saudi Diabetic Patients

Background: Preeclampsia is a life threatening state. Aerobic exercise has a beneficial effect on vascular endothelium function. Adropin is a newly discovered peptide that can increase by exercise and decreased in endothelial dysfunction. Objectives: Detecting the effect of practicing exercise on preeclampsia pathophysiology, and role of adropin. Patients and Methods: Twenty four adult female albino wistar rats were divided into 3 equal groups: group I: Sham-operated Time-mated pregnant rats (Sham), group II: Reduced uterine perfusion pressure pregnant rats (RUPP); placental ischemia was induced at gestation day (GD) 14 to mimic preeclampsia, and group III: exercise treated reduced uterine perfusion pressure pregnant rats (Ex-RUPP); swimming started from GD1 till the end of pregnancy period, 1h/day, 6 days/week added to preeclampsia induction. Maternal arterial blood pressure, micro-albuminuria, serum urea, creatinine and calculated glomerular filtration rate (GFR), plasma insulin, glucose and calculated HOMA-IR and placental eNOS, adropin, soluble fms–like tyrosine kinase 1 (sFlt-1), malondialdehyde (MDA), total antioxidant capacity (TAC), and TNF-α were measured. Placental and fetal tissues were weighed and placenta was histo-pathologically assessed. Results: Aerobic exercise during pregnancy caused significant reductions in all blood pressure values at GD17 and 19, serum urea, creatinine, micro-albuminuria, placental anti-angiogenic sflt-1, MDA, TNF-α, plasma glucose, insulin and HOMA-IR. In addition, exercise significantly increased the calculated creatinine clearance, placental eNOS and placental adropin, placental weight, fetal weight and number. Apoptotic trophoblasts and neutrophil aggregates were absent. Adropin was significantly positive correlated with eNOS together with a significant negative correlation to mean arterial blood pressure at GD19, sflt-1, MDA, insulin and HOMA-IR. Conclusion: Aerobic exercise, through increasing adropin level, was able to restore the angiogenic balance, and to decrease the oxidative stress, and inflammatory and insulin resistance states, thus improving endothelial function. This was reflected in improvement in the renal functions, blood pressure reduction with better maternal and fetal outcome.

Changes in serum adropin, salusin alpha and salusin beta, vaspin, and preptin in hyperemesis gravidarum

Purpose: To investigate serum levels of adropin, salusin alpha and salusin beta, vaspin, and preptin in pregnant women with hyperemesis gravidarum (HG) and uncomplicated pregnancies. Materials and Methods: Thirty-three pregnant women with HG (group 1) and 30 pregnant women with uncomplicated pregnancies (group 2) who were referred to the University Obstetrics-Gynecology clinic were enrolled in this present study. Fasting serum samples were obtained and measured for adropin, salusin alpha and salusin beta, vaspin, and preptin. The hormones levels were studied by using ELISA method. Results: Statistically significant difference was found between groups 1 and 2 according to adropin, salusin alpha and salusin beta, vaspin, and preptin levels (all p Conclusion: This study suggests a possible role of these peptides, which may clarify the etiopathogenesis of HG.