Serum Adropin Research Articles

Adropin in women with polycystic ovary syndrome.

Women with polycystic ovary syndrome (PCOS) frequently develop metabolic complications. Among the newly found factors responsible for metabolic disorders, adropin seems to be of a great significance. In total 134 women aged 17-45 years were enrolled. The PCOS group consisted of 73 women, diagnosed on the basis of Executive Committee of the European Society of Human Reproduction and Embryology - American Society for Reproductive Medicine (ESHRE-ASRM) criteria. All PCOS women presented phenotype A of PCOS. The control group consisted of 61 women with regular menstrual cycles, matched for nutritional status. All women underwent anamnesis, physical examination, anthropometric measurements, abdominal and transvaginal ultrasound, and dual-energy X-ray absorptiometry (DXA). Serum adropin levels were determined by ELISA. Biochemical [fasting glucose and insulin, oral glucose tolerance test, lipid and sex hormone-binding globulin (SHBG)] and hormonal (testosterone, androstenedione, luteinizing hormone, follicle-stimulating hormone and oestradiol) measurements were performed. Insulin resistance indices [(Homeostasis Model Assessment for Insulin Resistance (HOMA-IR), Quantitative Insulin Sensitivity Check Index (QUICKI), Matsuda] and free androgen index (FAI) were calculated according to the standard formula. Serum adropin levels were lower in the PCOS group (0.475 ± 0.200 vs. 0.541 ± 0.220, p = 0.069), but the results were not statistically significant. Positive correlations among adropin and androstenedione levels were observed in the PCOS group (r = 0.27, p = 0.025). Women with PCOS have a different metabolic profile in comparison to women without this syndrome. We did not observe a statistically significant difference in adropin concentration between the PCOS and the healthy control group. Therefore, more studies regarding adropin in PCOS are needed.

Association between serum adropin level and coronary artery disease: a systematic review and meta-analysis.

Recent studies have found that adropin is associated with coronary artery disease (CAD). This meta-analysis sought to assess the relationship between serum adropin level and CAD. Online databases including the Cochrane Library, PubMed, EMbase, Ovid, CBM, CNKI, VIP and WanFang Data were electronically searched for the clinical study concerning the relationship between serum adropin levels and CAD, including acute myocardial infarction (AMI), unstable angina pectoris (UAP), and stable angina pectoris (SAP). Two reviewers independently screened literature, extracted data and assessed methodological quality of included studies. Standard mean difference (SMD) with its 95% confidence interval (CI) was used as the effect size in this study. Then meta-analysis was performed using RevMan 5.2 software. A total of seven articles involved 945 participants were included. The results indicated that serum adropin level in CAD group was lower than healthy control group (SMD =-2.44, P=0.0008). In the subgroup analysis, the levels of serum adropin in AMI group (SMD =-2.96, P<0.00001), UAP group (SMD =-2.09, P=0.0001) and SAP group (SMD =-1.23, P=0.007) were also lower than that of healthy control. Serum adropin level in patients with CAD was lower than healthy individuals, indicating that the decrease of adropin concentration might play an important role in the development of CAD.

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 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.

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.

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.

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.

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.

Association of serum adropin with the presence of atrial fibrillation and atrial remodeling.

Adropin, a newly identified regulatory protein encoded by Enho gene, suppressed tumor necrosis factor α-induced THP1 monocyte adhesion to human umbilical vein endothelial cells. In addition, inflammation is demonstrated to be involved in the mechanism of atrial fibrillation (AF). Atrial remodeling is correlated with the persistence and progression of AF. Adropin is hypothesized to correlated with AF and atrial remodeling. This study aims to determine the correlation of serum adropin and the presence of AF and remodeling. This study consisted of 344 AF patients and 210 healthy controls. AF patients were then divided into three subgroups of paroxysmal AF, persistent AF, and permanent AF. Serum adropin concentrations were examined using enzyme-linked immunosorbent assay method. Left atrial diameter (LAD) was measured to evaluate atrial remodeling. Decreased serum adropin concentrations were found in AF patients compared with healthy controls. Logistic regression analysis confirmed that serum adropin was inversely associated with the presence of AF (OR 0.218, 95% CI 0.15-0.316; P<0.001). Permanent AF patients had significantly reduced serum adropin concentrations compared with persistent and paroxysmal AF patients. There were decreased serum adropin concentrations in persistent AF group than those in paroxysmal AF group. Simple linear regression analyses showed that serum adropin in AF patients were negatively correlated with BMI, SBP, and LAD. Multiple stepwise regression analysis showed that LAD remained to be inversely associated with serum adropin (β=0.2, P=0.010). Serum adropin concentrations are inversely correlated with the presence of AF and atrial remodeling.

Effects of Probiotic Yogurt on Serum Omentin-1, Adropin, and Nesfatin-1 Concentrations in Overweight and Obese Participants Under Low-Calorie Diet.

Data on the effects of probiotics on adipokines such as omentin-1, nesfatin-1, and adropin are limited. The aim of this study was to evaluate the effects of probiotic yogurt along with a low-calorie diet (LCD) on serum omentin-1, adropin, and nesfatin-1 concentrations in obese and overweight individuals. Sixty obese or overweight individuals aged 20-50years old were involved in this randomized double-blind placebo-controlled clinical trial. Participants were randomly allocated into two groups to consume either probiotic yogurt containing Lactobacillus acidophilus La5, Bifidobacterium BB12, and Lactobacillus casei DN001 (108CFU/g each) (n = 30) or regular yogurt (n = 30) along with a LCD in both groups for 8weeks. Fasting blood samples were taken at baseline and after the 8-week intervention to determine related variables. A significant decrease in body fat percentage was observed in the probiotic group compared with the regular group after 8weeks (- 1.51 ± 069 vs - 0.88 ± 0.68%, P = 0.002). After the 8-week intervention, a significant difference in serum adropin concentration (6.04 ± 24.46 vs - 8.16 ± 24.66pg/ml, P = 0.03 and serum omentin-1 concentration (0.09 ± 1.51 vs - 1.5 ± 1.8ng/ml, P = 0.003) was observed between two groups. We did not observe any significant changes in nesfatin-1 and other anthropometric measures. Overall, probiotic yogurt for 8weeks among overweight or obese individuals along with LCD had beneficial effects on body fat percentage, serum omentin-1, and adropin concentration, but it did not have any effect on nesfatin-1 level.

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.

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.

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.

Preptin in women with polycystic ovary syndrome

Introduction: Polycystic ovary syndrome (PCOS) patients, frequently develop metabolic complications, such as insulin resistance (IR), impaired carbohydrate metabolism, dyslipidemia, obesity. Among the new markers responsible for metabolic disorders, preptin seems to be of great significance. Material: One hundred and thirty-four women aged 17–45 were enrolled. PCOS was diagnosed in 73 women on the basis of ESHRE-ASRM criteria. Non-PCOS group consisted of 61 women with regular menstruation matched for nutritional status. Methods: All women underwent anamnesis, physical examination, anthropometric measurements, the abdominal ultrasound examination, and dual energy X-ray absorptiometry (DXA). Serum adropin levels were determined by ELISA. Biochemical and hormonal (testosterone, androstenedione, LH, FSH, estradiol) measurements were also performed. Insulin resistance indices (HOMA, QUICKI, Matsuda) and free androgen index (FAI) were calculated with the test results according to the standard formula. For all comparisons, statistical significance was defined by p ≤ .05. Results: Serum preptin levels were significantly higher in the PCOS group. No significant correlations between preptin level and metabolic and hormonal markers were observed. The logistic regression analysis demonstrated that serum preptin level was an independent factor differentiating the two groups. Conclusions: Serum preptin levels were significantly higher in women with PCOS compared with controls. This peptide might be an independent predictor of PCOS in the future.

Adropin and circadian variation of blood pressure.

Nocturnal hypertension and non-dipping pattern are often associated with endothelial dysfunction. Previous studies suggested that adropin, a novel secreted energy homeostasis protein, has the unique ability to regulate endothelial cell function. This study aims to investigate the association between absolute night-time blood pressure (BP) and circadian BP pat-tern with serum adropin and high-sensitivity C-reactive protein (hsCRP) levels in patients with newly diagnosed untreated arterial hypertension. Twenty-four-hour ambulatory BP monitoring was recorded in 100 hypertensives (50 dippers, 50 non-dippers) and 50 healthy controls. Serum levels of adropin and hsCRP were measured and recorded. A strong correlation was found between night-time BP levels with adropin and hsCRP levels (p < 0.001). On the other hand, the non-dipper group demonstrated lower adropin levels compared to the dipper and normotensive groups: non dipper group, 2580 ± 457 pg/mL; dipper group, 3298 ± 530 pg/mL; normotensive group, 3681 ± 411 pg/mL; p < 0.001). HsCRP levels were significantly higher in the non-dipper group than in the two other groups (p = 0.017). In a multivariate logistic regression analysis, adropin (p = 0.012) and hsCRP (p = 0.039) were independently associated with a non-dipping pattern. Decreased adropin levels were found in the nocturnal hypertensive and non-dipper groups. Adropin and hsCRP were found to be independently associated with a non-dipping pattern. We suggest that decreased levels of adropin in non-dipper hypertensive patients might be associated with a longer duration of exposure to high BP. These results point to a possible future role of adropin in identifying hypertensive patients at higher risk of target organ damage.

SERUM ADROPIN LEVEL AND KIDNEY FUNCTIONS IN TYPE-II DIABETIC RAT MODEL WITH AND WITHOUT PIOGLITAZONE TREATMENT

Background: Diabetic nephropathy (DN) is the most common cause of end stage renal disease (ESRD), and the leading cause of death in diabetic patients. Treatment with thiazolidinediones, particularly pioglitazone, may ameliorate kidney deterioration. Moreover, several peptide hormones participate in maintaining metabolic homeostasis including the recently discovered adropin. Data regarding adropin-circulating levels in type II diabetes mellitus (T2DM) are still conflicting. Objective: This study was designed to determine pioglitazone effect on some metabolic and kidney function parameters in type II diabetic rat model, and to investigate the relationship between serum adropin and such parameters. Materials and methods: Thirty healthy adult male albino rats were used for this study. The rats were randomly and equally divided into three groups. Group-1; control group, group-2; type II diabetic group, and group-3; pioglitazone- treated diabetic group. Rats were examined for body weight, body mass index (BMI), adropin, glucose & insulin, insulin resistance (HOMA-IR), lipids profile, inflammatory cytokines [interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), plasminogen activator inhibitor-1 (PAI-1)], serum urea, creatinine, uric acid, angiotensin II, mean arterial blood pressure (MABP), urine flow rate, protein, creatinine, glomerular filtration rate (GFR), renal malondialdhyde (MDA) level, glutathione peroxidase (GSH‑Px), and superoxide dismutase (SOD) activities. Histopathological examinations for kidney tissues were also done. Results: The present study revealed that diabetic rats showed significantly lower serum adropin levels than controls. Diabetes also significantly increased serum glucose with insulin resistance, serum total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), serum IL-6, TNF-α, PAI-1, serum urea, creatinine, uric acid, angiotensin II , MABP, urine flow rate, protein and renal MDA [with significant negative correlation versus serum adropin] but significantly decreased serum insulin and high density lipoprotein-cholesterol (HDL-c), urine creatinine, GFR and renal SOD & GSH‑Px activities [with significant positive correlation versus serum adropin] together with deterioration of kidney histoarchitecture. Moreover, pioglitazon treatment resulted in a significant recovery in the above mentioned parameters in the treated diabetic group. Conclusion: Serum adropin concentration was negatively associated with the observed renal deterioration and may have a potential protective role, in addition to pioglitazone ameliorating effects, in diabetic nephropathy.

SERUM ADROPIN LEVEL AND KIDNEY FUNCTIONS IN TYPE-II DIABETIC RAT MODEL WITH AND WITHOUT PIOGLITAZONE TREATMENT

Background: Diabetic nephropathy (DN) is the most common cause of end stage renal disease (ESRD), and the leading cause of death in diabetic patients. Treatment with thiazolidinediones, particularly pioglitazone, may ameliorate kidney deterioration. Moreover, several peptide hormones participate in maintaining metabolic homeostasis including the recently discovered adropin. Data regarding adropin-circulating levels in type II diabetes mellitus (T2DM) are still conflicting. Objective: This study was designed to determine pioglitazone effect on some metabolic and kidney function parameters in type II diabetic rat model, and to investigate the relationship between serum adropin and such parameters. Materials and methods: Thirty healthy adult male albino rats were used for this study. The rats were randomly and equally divided into three groups. Group-1; control group, group-2; type II diabetic group, and group-3; pioglitazone- treated diabetic group. Rats were examined for body weight, body mass index (BMI), adropin, glucose & insulin, insulin resistance (HOMA-IR), lipids profile, inflammatory cytokines [interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), plasminogen activator inhibitor-1 (PAI-1)], serum urea, creatinine, uric acid, angiotensin II, mean arterial blood pressure (MABP), urine flow rate, protein, creatinine, glomerular filtration rate (GFR), renal malondialdhyde (MDA) level, glutathione peroxidase (GSH‑Px), and superoxide dismutase (SOD) activities. Histopathological examinations for kidney tissues were also done. Results: The present study revealed that diabetic rats showed significantly lower serum adropin levels than controls. Diabetes also significantly increased serum glucose with insulin resistance, serum total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), serum IL-6, TNF-α, PAI-1, serum urea, creatinine, uric acid, angiotensin II , MABP, urine flow rate, protein and renal MDA [with significant negative correlation versus serum adropin] but significantly decreased serum insulin and high density lipoprotein-cholesterol (HDL-c), urine creatinine, GFR and renal SOD & GSH‑Px activities [with significant positive correlation versus serum adropin] together with deterioration of kidney histoarchitecture. Moreover, pioglitazon treatment resulted in a significant recovery in the above mentioned parameters in the treated diabetic group. Conclusion: Serum adropin concentration was negatively associated with the observed renal deterioration and may have a potential protective role, in addition to pioglitazone ameliorating effects, in diabetic nephropathy.

Serum adropin levels are decreased in Chinese type 2 diabetic patients and negatively correlated with body mass index.

Adropin has been identified as potent regulatory hormone implicated in insulin sensitivity and the maintenance of energy homeostasis. The aim of current study was to investigate serum adropin concentrations of type 2 diabetes mellitus (T2DM) patients in the fasting status, especially those overweight/obese and evaluate the relationships between adropin levels and metabolic parameters. A total of 116 T2DM patients and 60 controls with normal glucose tolerance (NGT) were recruited to the study. Adropin concentration was determined using commercial ELISA kits. Anthropometric characteristics were collected and biochemistry, glycosylated hemoglobin A1c (HbA1c) and fasting insulin (FIns) were detected by clinical laboratory. Insulin resistance was estimated by homeostasis model 2 assessment of insulin resistance (HOMA2-IR). Serum adropin levels in Chinese T2DM patients were decreased compared with the controls [3.8 (3.0-5.5) vs. 5.5 (3.7-7.9) ng/mL, p < 0.01]. Meanwhile, overweight/obese patients had more considerably reduced levels of adropin. Adropin level was negatively correlated with body mass index (BMI), high-sensitive C reactive protein (hs-CRP), triglycerides (TG), fasting plasma glucose (FPG), FIns, HOMA2-IR and HbA1c, while positively with high-density lipoprotein cholesterol (HDL-C) in study participants (p < 0.01). The correlations of adropin with glucolipid variables (TG, HDL-C, FPG, FIns, HOMA2-IR, HbA1c) still existed after adjusting the effect of BMI. Besides, HOMA2-IR and HbA1c were independent factors associated with serum adropin levels. Binary logistic regression analyses showed that adropin was significantly associated with T2DM after removing confounding factors (p < 0.01). Receiver operating characteristic (ROC) curve demonstrated adropin concentration of 5.8 ng/mL could be used as a possible optimal cut-off value to identify T2DM from non-T2DM with sensitivity of 81.9% and specificity of 46.7%. Serum adropin concentrations are decreased in Chinese T2DM patients, especially those overweight/obese. Adropin, associated with glucolipid homeostasis and insulin sensitivity, may implicate in the pathogenesis of T2DM.