Asprosin Research Articles

Asprosin aggravates nonalcoholic fatty liver disease via inflammation and lipid metabolic disturbance mediated by reactive oxygen species.

Asprosin (ASP) is a newly-identified adipokine and plays important roles in energy metabolism homeostasis. However, there is no report on whether and how ASP is involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Therefore, in the study, we investigated the protective effects of ASP-deficiency on the liver in the NAFLD model mice and the detrimental effects of ASP treatment on the human normal hepatocytes (LO2 cell line). More important, we explored the underlying mechanism from the perspective of lipid metabolism and inflammation. In the in vivo experiments, our data showed that the ASP-deficiency significantly alleviated the high-fat diet-induced inflammation and NAFLD, inhibited the hepatic fat deposition and downregulated the expressions of fat acid synthase (FASN), peroxisome proliferator-activated receptor γ (PPARγ) and forkhead box protein O1 (FOXO1); moreover, the ASP-deficiency attenuated the inflammatory state and inhibited the activation of the IKK/NF-κBp65 inflammation pathway. In the in vitro experiments, our results revealed that ASP treatment caused and even exacerbated the injury of LO2 cells induced by FFA; In contrast, the ASP treatment upregulated the expressions of PPARγ, FOXO1, FASN, ACC and acyl-CoA oxidase 1 (ACOX1) and elevated the reactive oxygen species (ROS) levels. Accordingly, these results demonstrate that ASP causes NAFLD through disrupting lipid metabolism and promoting the inflammation mediated by ROS.

Asprosin contributes to pathogenesis of obesity by adipocyte mitophagy induction to inhibit white adipose browning in mice.

Asprosin (ASP) is a newly discovered adipokine secreted by white adipose tissue (WAT), which can regulate the homeostasis of glucose and lipid metabolism. However, it is not clear whether it can regulate the browning of WAT and mitophagy during the browning process. Accordingly, this study aims to investigate the effects and possible mechanisms of ASP on the browning of WAT and mitophagy in vivo and in vitro. In in vivo experiments, some mouse models were used including adipose tissue ASP-specific deficiency (ASP-/-), high fat diet (HFD)-induced obesity and white adipose browning; in in vitro experiments, some cell models were also established and used, including ASP-deficient 3T3-L1 preadipocyte (ASP-/-) and CL-316243 (CL, 1 µM)-induced browning. Based on these models, the browning of WAT and mitophagy were evaluated by morphology, functionality and molecular markers. Our in vivo data show that adipose tissue-specific deletion of ASP contributes to weight loss in mice; supplementation of ASP inhibits the expressions of browning-related proteins including UCP1, PRDM16 and PGC1ɑ during the cold exposure-induced browning, and promotes the expressions of mitophagy-related proteins including PINK1 and Parkin under the conditions of whether normal diet (ND) or HFD. Similarly, our in vitro data also show that the deletion of ASP in 3T3-L1 cells significantly increases the expressions of the browning-related proteins and decreases the expressions of the mitophagy-related proteins. These data demonstrate that ASP deletion can facilitate the browning and inhibit mitophagy in WAT. The findings will lay an experimental foundation for the development of new drugs targeting ASP and the clinical treatment of metabolic diseases related to obesity.

Role of asprosin and meteorin-like peptide in progression of actinic keratosis to squamous cell carcinoma

ABSTRACT Squamous cell carcinoma (SCC) often develops from an underlying premalignant lesion. Factors that affect the progression of actinic keratosis (AK) to invasive SCC are not fully known. Asprosin (ASP) and meteorin-like peptide (METRNL) are adipokines that are involved primarily in glucose metabolism. We investigated the expression of ASP and METRNL in AK and SCC to evaluate the role of these adipokines in the development of SCC. We used 15 SCC specimens, 12 AK specimens and 12 healthy control skin specimens. ASP and METRNL protein expression in tumor and surrounding tissue was evaluated using immunohistochemistry. ASP expression in tumor tissue was significantly greater in the SCC group than in the control and AK groups, but it did not differ significantly between the AK and control groups. A positive correlation was observed for both ASP and METRNL expressions between tumor tissue and adjacent epidermis, hair follicles, sebaceous gland, eccrine gland, inflammatory cells and vascular structures. ASP and METRNL may exert pro-tumor effects toward development of invasive SCC. The expression intensity of ASP and METRNL can be used as a biomarker of risk of progression to SCC.

Exercise-induced effects on asprosin and indices of atherogenicity and insulin resistance in males with metabolic syndrome: a randomized controlled trial

Metabolic syndrome (MetS) development is associated with insulin resistance and obesity, with the progression of visceral adipose tissue playing a crucial role. Excessive adipose tissue is accompanied by an increase in the asprosin (ASP), which is responsible for carbohydrate metabolism and the regulation of hunger and satiety. Exercise affects the release of ASP, which may regulate metabolism accordingly. Due to the inconclusive results of the effect of exercise on ASP concentration in men with MetS, 12-week interventions were carried out in the following groups: EG1—aerobic training (n = 21, age: 34.21 ± 6.06, WC; waist circumference: 114.7 ± 10.93) and EG2—a combination of aerobic and resistance training (n = 21, age: 37.37 ± 7.08, WC: 114.8 ± 11.64) and compared with a control group (CG) of men with MetS without any intervention (n = 20, age: 38.26 ± 7.43, WC: 115.3 ± 10.54). Body composition, indicators of carbohydrate-lipid metabolism, and ASP were assessed four times: before the intervention, at 6 and 12 weeks of training, and 4 weeks after the training sessions. A comparison of the intervention influence on changes in the analyzed variables between the groups was performed using ANOVA test for dependent groups with post-hoc comparison. The effect size (ES) was also assessed using squared eta (η2). The implementation of aerobic training resulted in a decrease in ASP concentration (p = 0.03) within 6 weeks of the intervention, while in the CG a gradual increase in ASP was confirmed (p < 0.001). Aerobic-resistance training did not induce significant changes in ASP concentration but resulted in an increase in fat-free mass/fat mass (FFM/FM) ratio (p < 0.001), and a decrease (p = 0.04) in Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Changes in the visceral adipose tissue level indicate a gradual decrease in both the EG1 (p = 0.01) and EG2 (p = 0.04) groups. Both aerobic and aerobic-resistance exercises may have a regulatory effect, mainly by reducing visceral adipose tissue, on the improvement of metabolic disorders.

Elevated Asprosin Levels in Breast Cancer: Insights from a Comparative Study.

Background: Breast cancer (BC) is the most common type of cancer in women. Diagnosis in the early stage is very important for cancer treatment. There is no good biomarker to diagnose BC in T1-T2 or N0 stage. This study aimed to evaluate asprosin (ASP) levels of BC compared with non-cancer. Materials and Methods: An enzyme-linked immunosorbent assay was used to evaluate serum ASP levels in 40 patients with BC and 40 healthy women. The cancer group included T1-T4, N1-N3, and M0-M1 patients. T stages were divided into groups as T1-T2 and T3-T4. N stages were divided into groups as N (0) and N (+). Results: ASP showed good discrimination (area under the curve = 0.767, 95% confidence interval: 0.657-0.878) between the BC group and the healthy group and acceptable discriminating ability (sensitivity = 0.825; specificity = 0.750) at the optimal cutoff value of 1.82 ng/mL. ASP indicated no difference for T, N, and M stages (p = 0.919, p = 0.859, and p = 0.225, respectively). There was a significant difference between grades within cancer patients in terms of ASP (p = 0.025). Conclusions: These findings provide evidence of a potential association between elevated ASP levels and the presence of BC. The observed higher levels of ASP in women with BC compared with healthy individuals suggest that ASP could potentially serve as a biomarker for distinguishing between the two groups. These results may contribute to our understanding of the potential role of ASP in BC detection and highlight its potential as a diagnostic marker. Further studies are required to establish whether ASP can be used to diagnose BC.

Subfatin, asprosin, alamandine and maresin-1 in cerebral ischemia, intracranial and subarachnoid hemorrhages.

Cerebrovascular diseases (CVDs) remain an important public health issue due to the increasing number of deaths worldwide. Changes in the synthesis and release of peptides in CVDs may play an important role in elucidating the physiopathology of the disease. Therefore, this study was to investigate the fate of maresin-1 (MaR-1), subfatin (SUB), asprosin (ASP), and alamandine (ALA) levels in patients with cerebral infarction (CI), intracranial hemorrhage (ICH), subarachnoid hemorrhage (SAH) evaluated within the scope of CVDs, and voluntary healthy controls. The study participants were divided into 4 groups: CI patients, ICH patients, SAH patients, and healthy volunteers. The diagnosis of CVDs was made based on the National Institutes of Health Stroke Scale (NIHSS), Intracerebral Hemorrhage Score (ICHS), Botterel-Hunt-Hess Scale (BHHS), and cranial computed tomography (CT). The levels of MaR-1 (ng/mL), SUB (ng/mL), ASP (ng/mL), and ALA (pg/mL) in the blood samples collected from the participants were studied using the ELISA method. Other parameters included in the study were obtained from the patient records of our hospital. The comparison of MaR-1 [(control 1.38 ± 0.14), SAH (0.98 ± 0.087), CI (0.67 ± 0.04), ICH (0.51 ± 0.03)], SUB [(control (13.2 ± 1.4), SAH (10.1 ± 1.2), CI (7.9 ± 0.8), ICH (5.8 ± 0.5)], and ALA [(control (67.2 ± 7.9), SAH (58.2 ± 4.3), CI (42.1 ± 3.7), and ICH (34.2 ±3.9)] values revealed a significant decrease compared to the control values. The comparison of the ASP values of SAH, CI, and ICH patients and control values (11.6 ± 1.2) showed significantly higher asprosin values in SAH (13.8 ± 1.1), CI (15.4 ± 1.2) and ICH (28.9 ± 2.8) patients. Similarly, systolic blood pressure (SBP), diastolic blood pressure (DBP), and glucose levels of CKD patients were also high. Decreased MaR-1, SUB, ALA and increased ASP compared to the control values may play a role in the physiopathology of these diseases. MaR-1, SUB, ALA, and ASP differences between SAH, CI and ICH patients may also guide clinicians along with SBP, DBP and glucose values.

Carvacrol protects rat liver exposed to formaldehyde by regulating oxidative stress, and asprosin and subfatin hormones

ABSTRACT Toxic doses of formaldehyde (FA) can cause oxidative damage and impair energy metabolism. Asprosin (ASP) and subfatin (SUB) are adipokines produced by adipose tissue that help regulate energy metabolism. We investigated the effects of carvacrol (CAR), an antioxidant with hepatoprotective properties, on ASP and SUB in rats exposed to FA using immunohistochemistry and biochemistry. We used 42 male Wistar albino rats divided into six groups of seven: group 1, untreated control; group 2, FA (10 ppm FA by inhalation 8 h/day, 5 days/week); group 3, CAR-20 (20 mg/kg); group 4, CAR-40; group 5, FA (10 ppm FA by inhalation 8 h/day, 5 days/week) + CAR-20 (20 mg/kg); group 6, FA (10 ppm FA by inhalation 8 h/day, 5 days/week) + CAR-40 (40 mg/kg). Levels of ASP and SUB, and total oxidant status (TOS) and total antioxidant status (TAS) in blood and liver tissue were measured using ELISA. ASP and SUB immunoreactivity was assessed using immunohistochemistry. The number of apoptotic cells was determined using the TUNEL method. The number of apoptotic cells in group 2 was increased compared to group 1. TOS in group 2 was increased compared to group 1. The numbers of apoptotic cells and TOS in group 3 were decreased compared to group 1. TOS was decreased in group 6 compared to group 2, but TOS was increased compared to group 1. We found ASP and SUB immunoreactivity in the liver. All alterations were reversed by addition of CAR. It appears that FA disrupts energy metabolism and CAR ameliorates the destructive effects of FA when used at appropriate doses, although CAR might be harmful at high doses.

Apelin-13 and Asprosin in Adolescents with Anorexia Nervosa and Their Association with Psychometric and Metabolic Variables

IntroductionAnorexia nervosa (AN) is a widespread, metabo-psychiatric disorder with high relapse rates, comorbidity, and mortality. Many regulatory proteins and neurohormones studied to date play essential roles in the etiopathogenesis of eating disorders and the maintenance of psychopathological symptoms. Nevertheless, the regulatory and pathophysiological mechanisms of AN are still poorly understood.ObjectivesThe present study aimed to investigate the plasma levels of asprosin (ASP) and apelin-13 (APE-13) in malnourished (AN1) and partially cured (AN2) adolescent patients with AN. Correlations between protein levels and several dimensions of AN symptomatology, such as eating disorder, depressive, and obsessive compulsive symptoms, were investigated.MethodsSixty-four patients aged 11–18 years admitted to the Department of Child and Adolescent Psychiatry in the acute phase of AN participated in the study. Between the 1st and 3rd days of admission, patients with AN (AN1) underwent psychometric evaluation, height and weight assessment, and 15 mL of blood was drawn. The same procedures were repeated at a second time point about 11.2 ± 2.3 weeks later, after partial normalization of body weight on the day of discharge (AN2). The control group (CG) normal-weight girls with no history of psychiatric disorders, recruited from among the students of a local school. The Eating Attitudes Test (EAT-26), Beck Depression Inventory (BDI) Hamilton Depression Scale (HAMD) and Yale–Brown Obsessive Compulsive Scale (CYBOCS), were used to assess eating disorder symptoms, depression, obsessions and compulsions. Patients were included in a nutritional rehabilitation program. Daily caloric intake was 2000–2500 kcal and was gradually increased to 3500–4000 kcal depending on weight gain (1.0–1.5 kg per week).ResultsAPE-13 levels were higher in the AN1 group than in the post-realimentation and the CG group. APE-13 levels were independent of insulin and glucose levels. Plasma ASP levels increased with increasing body weight in patients with AN, correlating with the severity of eating disorder symptoms in emaciation.Image:Image 2:Image 3:ConclusionsThe presented data suggest that APE-13 and ASP may be AN’s biomarkers-regulation of eating behavior by APE-13 and ASP, the close relationship between them and emotional behavior, and changes in neurohormone levels in patients with eating and affective disorders seem to support these hypotheses. Moreover, their plasma levels seem to be related to the severity of psychopathological symptoms of eating disorders.Disclosure of InterestNone Declared

Betatrophin, elabela, asprosin, glucagon and subfatin peptides in breast tissue, blood and milk in gestational diabetes

ABSTRACT We investigated the presence of asprosin (ASP), betatrophin, elabela (ELA), glucagon and subfatin (SUB) in the milk of mothers with gestational diabetes mellitus (GDM) and compared their levels with blood levels. We also investigated whether these peptides are synthesized by the breast. We investigated 12 volunteer mothers with GDM and 14 pregnant non-GDM control mothers. The peptides were measured using ELISA and their tissue localization was determined using immunohistochemistry. Breast milk contains ASP, betatrophin, ELA, glucagon and SUB. The amount of the peptides ranged from highest to the lowest in colostrum, transitional milk and mature milk. The amount of peptides in the milk was greater than for blood. The peptides, except for ELA, were increased in milk and blood by GDM. Betatrophin and ELA are synthesized in the connective tissue of the breast. ASP, glucagon and SUB are synthesized in the alveolar tissue of the breast. These peptides in breast milk may contribute to the development of the gastrointestinal tract of newborns and infants.

Asprosin aggravates vascular endothelial dysfunction via disturbing mitochondrial dynamics in obesity models.

The aim of the study was to investigate the contribution of asprosin (ASP), a fasting-induced hormone involved in metabolic disorders, to vascular endothelial dysfunction in obesity models. Primary rat thoracic aortic endothelial cells treated with palmitic acid and mice fed with a high-fat diet (HFD) were used as the obesity models. The role and mechanism of ASP in endothelial dysfunction were investigated by the means of morphologic, functional, and genetic analysis. ASP aggravated the endothelial dysfunction induced by either palmitic acidin vitro or an HFD in vivo, characterized as the impairment of endothelium-dependent vasodilation, reduction of nitric oxide levels, elevation of malondialdehyde levels, and inhibition of phosphoinositide 3-kinase-AKT-endothelial nitric oxide synthase signaling. However, adipose conditional knockout of ASP or ASP neutralization significantly alleviated the endothelial dysfunction induced by an HFD. Mechanistically, ASP enhanced mitochondrial fission, and inhibition of the fission through knockdown of dynamin-related protein 1 (a fission-hallmark factor) rescued the endothelial dysfunction and the disturbance to mitochondrial dynamics induced by ASP. The findings demonstrate that ASP causes and even exacerbates vascular endothelial dysfunction through promoting mitochondrial fission in obesity, suggesting that ASP can act as an early predictive marker of blood vessel dysfunction and become a novel potential therapeutic target for obesity-related cardiovascular diseases.

Angiogenesis-Browning Interplay Mediated by Asprosin-Knockout Contributes to Weight Loss in Mice with Obesity.

Asprosin (ASP) is a recently identified adipokine secreted by white adipose tissue (WAT). It plays important roles in the maintenance of glucose homeostasis in the fasting state and in the occurrence and development of obesity. However, there is no report on whether and how ASP would inhibit angiogenesis and fat browning in the mouse adipose microenvironment. Therefore, the study sought to investigate the effects of ASP-knockout on angiogenesis and fat browning, and to identify the interaction between them in the ASP-knockout mouse adipose microenvironment. In the experiments in vivo, the ASP-knockout alleviated the obesity induced by a high fat diet (HFD) and increased the expressions of the browning-related proteins including uncoupling protein 1 (UCP1), PRD1-BF-1-RIZ1 homologus domain-containing protein-16 (PRDM16) and PPAR gamma coactivator 1 (PGC1-α) and the endothelial cell marker (CD31). In the experiments in vitro, treatment with the conditional medium (CM) from ASP-knockout adipocytes (ASP-/--CM) significantly promoted the proliferation, migration and angiogenesis of vascular endothelial cells, and increased the expressions of vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor 2 (VEGFR2) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/endothelial nitric oxide synthase (eNOS) pathway proteins. In addition, the treatment with CM from endothelial cells (EC-CM) markedly reduced the accumulation of lipid droplets and increased the expressions of the browning-related proteins and the mitochondrial contents. Moreover, the treatment with EC-CM significantly improved the energy metabolism in 3T3-L1 adipocytes. These results highlight that ASP-knockout can promote the browning and angiogenesis of WAT, and the fat browning and angiogenesis can interact in the mouse adipose microenvironment, which contributes to weight loss in the mice with obesity.

Asprosin Exacerbates Endothelium Inflammation Induced by Hyperlipidemia Through Activating IKKβ-NF-κBp65 Pathway.

Vascular endothelium dysfunction caused by endothelium inflammation is a trigger of numerous cardiovascular diseases. Vascular endothelium inflammation often occurs in patients with obesity. Asprosin (ASP) derived from white adipose tissue plays important roles in maintaining glucose homeostasis. However, effect of ASP on the vascular endothelium inflammation induced by hyperlipidemia and its underlying mechanism remains largely unclear. In this study, models of vascular endothelium inflammation were established to investigate the effect of ASP on the endothelium inflammation both in vivo and in vitro. Our data in vivo showed that recombinant ASP or high-fat diet (HFD) significantly increased the circulating levels of IL-6 and TNF-α and enhanced the adhesion of macrophages to endothelia characterized by the expression increase of CD68, ICAM-1, and VCAM-1 in rats. However, neutralization of ASP with an ASP specific antibody (AASP) significantly antagonized the changes induced by HFD. Similarly, our data in vitro also showed that ASP treatment elevated the expressions of IL-6, TNF-α, and ICAM-1 as well as VCAM-1. More important, our data revealed that the pro-inflammation effect of ASP was achieved by activating the IKKβ-NF-κBp65 pathway other than the oxidative stress pathway both in vivo and in vitro. In conclusion, our results demonstrate that ASP is a pro-inflammation player in the obesity-associated endothelium dysfunction. The findings would provide a novel target for the prevention and treatment of obesity-related cardiovascular diseases.

Use of asprosin and subfatin for differential diagnosis of serous ovarian tumors

ABSTRACT Asprosin (ASP) and subfatin are hormones that regulate glucose metabolism. The role of ASP and subfatin in serous ovarian tumors has not been investigated. We investigated the expression of subfatin and asprosin in 30 serous benign, 30 serous borderline, 30 malignant and 30 control ovarian tissues. We investigated ASP and subfatin immunoreactivity and quantification was achieved using an ELISA method. ASP and subfatin were localized in the epithelial parts of normal ovarian tissues; however, in cancer tissues, immunoreactivity was detected in the parenchymal areas. Biochemical analysis of ovarian tissues revealed significantly decreased ASP and subfatin compared to the control. We propose that ASP and subfatin are promising candidates for biomarkers to distinguish serous benign, serous borderline and malignant ovarian cancers.

Apelin-13 and Asprosin in Adolescents with Anorexia Nervosa and Their Association with Psychometric and Metabolic Variables.

Anorexia nervosa (AN) is a widespread, metabo-psychiatric disorder with high relapse rates, comorbidity, and mortality. Many regulatory proteins and neurohormones studied to date play essential roles in the etiopathogenesis of eating disorders and the maintenance of psychopathological symptoms. Nevertheless, the regulatory and pathophysiological mechanisms of AN are still poorly understood. In the presented study, the plasma levels of apelin-13 (APE-13) and asprosin (ASP), as well as carbohydrate metabolism parameters and psychometric parameters, were evaluated in low-weight adolescent female patients with AN (AN1), after partial weight normalization (AN2) and in an age-matched healthy control group (CG) were evaluated. APE-13 levels were higher in the AN1 group than in the post-realimentation and the CG group. APE-13 levels were independent of insulin and glucose levels. Plasma ASP levels increased with increasing body weight in patients with AN, correlating with the severity of eating disorder symptoms in emaciation. The presented data suggest that APE-13 and ASP may be AN’s biomarkers-regulation of eating behavior by APE-13 and ASP, the close relationship between them and emotional behavior, and changes in neurohormone levels in patients with eating and affective disorders seem to support these hypotheses. Moreover, their plasma levels seem to be related to the severity of psychopathological symptoms of eating disorders.

Diet and exercise interventions reduce serum asprosin and the corresponding hypothalamic– pituitary–gonad-axis dysfunction in obese men

Background: Asprosin (ASP) is a recently discovered adipocyte factor that participates in glucose metabolism and inflammatory reactions. Recent findings suggest that it may be involved in the regulation of sex hormone secretion in the hypothalamic-pituitary-gonad (HPG) axis, but no studies have been reported in related populations. The purpose of this study was to evaluate the changes in serum ASP levels in healthy men and obese men, as well as before and after exercise weight loss, and to investigate male hypogonadism, insulin resistance, inflammatory response, and relationships induced by ASP and obesity. Methods: Thirty-eight young male volunteers were recruited and divided into a normal group (n = 20) and an obese group (n = 18) according to their body mass index. Fourteen of the obese men underwent a 14-week exercise and diet intervention (first 8 weeks of aerobic exercise at 60%–70% HRmax for 30–50 min/4 days a week). Beginning at week 9, the intensity was increased to 75% HRmax. Participants in the obese groups maintained a calorie-restricted diet throughout the study period. Results: Serum ASP levels in the obese group were significantly higher than those in the normal group, and serum gonadotropin-releasing hormone (GnRh), luteinizing hormone (LH), and testosterone (T) levels were decreased. After 14 weeks of exercise and diet intervention, serum ASP decreased significantly, the levels of body weight, lean body weight, body fat rate, fasting insulin (FINS), homeostatic model assessment for insulin resistance, TNF-α, IL-6, and IL-1β decreased significantly, and the serum GnRH, LH, and T levels increased significantly. ASP was positively correlated with body weight, body fat percentage, FINS, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β and negatively correlated with relative lean body weight and serum LH and T levels. Conclusion: The serum ASP levels were increased in obese men compared with those of normal weight individuals, resulting in a chronic inflammatory reaction, high serum insulin, and HPG axis injury. Fourteen weeks of exercise and diet intervention effectively alleviated this phenomenon. It has been speculated that ASP might regulate male reproductive function by regulating the inflammatory response and insulin sensitivity.

Asprosin and meteorin-like protein immunoreactivity in invasive ductal breast carcinoma stages

AimThe study aimed to investigate asprosin (ASP) and meteorin-like (METRNL) protein immunoreactivity in invasive ductal breast cancer. Materials and methodsOverall, 60 cases of invasive ductal breast cancer (20 cases each of Grade 1, 2 and 3) were evaluated in addition to 20 normal breast tissues obtained from the Pathology Department Archive. ASP and METRNL expressions were assessed using immunohistochemical staining and visualised under a light microscope. ResultsThere was a significant difference in ASP and METRNL immunoreactivity among all the groups included in the study (p < 0.001). Cancer tissues with Grade 1, 2 and 3 showed a significant increase in ASP and METRNL immunoreactivity compared with the control group; however, no significant difference was noted among the cancer tissues with Grade 1, 2 and 3. ConclusionsASP and METRNL immunoreactivity increased at the cellular level in invasive ductal breast cancer, but there was no difference in immunoreactivity among the breast cancer grades.

Expression of asprosin in rat hepatic, renal, heart, gastric, testicular and brain tissues and its changes in a streptozotocin-induced diabetes mellitus model

In this study, we aimed to investigate the presence of asprosin (ASP) in the liver, kidneys, heart, stomach, testicles and brain and to determine the serum and tissue asprosin levels in diabetic rats. A total of 14 male Wistar Albino rats were divided into two groups, each containing 7 rats: (I) control group and (II) experimental diabetes group. Control rats received no treatment and the rats in the experiment group received single-dose of streptozotocin (STZ) (50 mg/kg) dissolved in 0.1 M sodium citrate buffer (pH: 4.5) intraperitoneally. Serum levels of asprosin were measured using ELISA method. The presence of asprosin in hepatic, renal, cardiac, gastric, testicular and brain tissues was investigated using immunohistochemical staining. Asprosin was detected in hepatocytes in the liver, cortical distal tubule cells in the kidney, cardiomyocytes in heart, surface epithelial cells of stomach fundus, interstitial Leydig cells in testes and cortical neurons of the brain. Compared to control group, it was found that diabetic rats had decreased asprosin levels in liver, kidney and heart tissues, increased levels in gastric and testicular tissues and no significant changes in brain tissue. Serum asprosin levels of diabetic rats were found to be decreased compared to the control group.This is the first study in the literature that reports the presence of asprosin in liver, kidney, heart, stomach, testis and brain tissues in rats. The aim of the study is to determine the presence of ASP, a newly discovered adipokine, in various tissues and to examine tissue and serum level changes in STZ-induced diabetes.

Study the Association of Asprosin and Dickkopf-3 with KIM-1, NTpro-BNP, GDF-15 and CPP among Male Iraqi with Chronic Kidney Disease.

In chronic kidney disease (CKD), kidneys develop injured over time and don’t work properly as in the kidneys for healthy people. At what time the kidneys cannot blood clean, further liquids stay and wastes in the body and which leads to many problems in health, such as high blood pressure (BP) and cardiovascular disease (CVD). In current study, we attempt to examine the association of asprosin (APN) and dickkopf-3 (DKK-3) with kidney injury molecule-1 (KIM-1), N-terminal pro-brain natriuretic peptide (NTpro-BNP), growth differentiation factor 15 (GDF-15) and copeptin (CPP) among male Iraqi with CKD. Methods: serum APN, DKK-3, KIM-1, NTpro-BNP, GDF-15 and CPP were determined by ELISA technique in 40 healthy controls (HCs) and 44 male patients with CKD, from the Al-Fallujah teaching hospital were recorded in this paper, serum concentrations of urea, creatinine and estimated glomerular filtration rate (eGFR) were measured by colorimetric methods Results: serum APN and DKK-3 were importantly greater in CKD males than in HCs (P

Can novel adipokines, asprosin and meteorin-like, be biomarkers for malignant mesothelioma?

ABSTRACTMalignant mesothelioma (MM) is a rare tumor of serous surfaces that has a poor prognosis. Cancer is a multistage process by which cells undergo metabolic and behavioral changes that cause excessive and untimely proliferation. Asprosin (ASP) and meteorin-like (METRNL) are two peptides associated with glucose and energy metabolism. We used immunohistochemistry to investigate whether these peptides could be biomarkers for diagnosis and treatment of MM. We reviewed 30 cases of MM and 30 cases of reactive mesothelial hyperplasia (RMH); we used the cases with RMH as control group. The specimens were examined using immunohistochemical staining for ASP and METRNL. ASP and METRNL immunoreactivity was more prominent in the MM specimens than the RMH specimens. Therefore, ASP and METRNL potentially could be used as markers for differentiating MM from benign diseases.

Asprosin improves the survival of mesenchymal stromal cells in myocardial infarction by inhibiting apoptosis via the activated ERK1/2-SOD2 pathway

AimsSeveral adipokines have been proven to improve the therapeutic efficacy of mesenchymal stromal cells (MSCs) when used to treat ischemic heart disease. Asprosin (ASP) is a newly-discovered adipokine. ASP might also predict the severity of coronary pathology. We investigated the role of ASP on MSCs and the effects of ASP-pretreated MSCs on myocardial infarction (MI). Main methodsMSCs were labelled with a lentivirus carrying green fluorescent protein (GFP). For in vivo study, after pretreatment with vehicle or ASP, MSCs were injected into infarcted hearts. Cardiac function and fibrosis were then evaluated 4 weeks after the induction of MI and survival of MSCs evaluated after 1 week. MSCs proliferation and migration were investigated after ASP treatment in vitro. MSCs apoptosis induced by hydrogen peroxide (H2O2) was assessed using flow cytometry. Key findingsCompared to vehicle-pretreated MSCs, ASP-pretreated MSCs significantly improved the left ventricular ejection fraction (LVEF), and inhibited myocardial fibrosis 4 weeks after MI. ASP pretreatment may have promoted homing of transplanted MSCs. In vitro results showed that ASP had no significant effect on MSC proliferation and migration, but protected these cells from H2O2-induced apoptosis. Among 21 molecules associated with antioxidation and cell death, the antioxidant enzyme SOD2 was significantly upregulated by ASP. Furthermore, ASP treatment inhibited H2O2-induced ROS generation and apoptosis via the activated ERK1/2-SOD2 pathway. SignificanceThis is the first evidence that ASP can regulate MSCs function and enhance MSCs therapy for ischemic heart disease. Furthermore, we demonstrate that ASP protects MSCs from oxidative stress-induced apoptosis via the ERK1/2-SOD2 pathway.