Asprosin Levels Research Articles

Effect of synbiotic supplementation on asprosin level in high fat diet-induced metabolic disorder in pregnant rats

Synbiotic supplementation can improve metabolic disorders. The aim of this study was to assess the impact of synbiotic supplementation on the levels of asprosin, lipid profile, glucose, and insulin resistance in pregnant rats fed a high-fat diet (HFD). Rats were divided into three groups: control group (fed base chow), HFD group, and HFD + synbiotic group. Levels of blood glucose, total cholesterol, triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), insulin, and asprosin levels were measured. Birth weight of offspring in the HFD + synbiotic group was significantly lower than in the HFD group. Similarly, serum asprosin, insulin, insulin resistance, TG and total cholesterol levels in the HFD + symbiotic group were significantly lower than in the HFD group. Asprosin levels had a significant and positive correlation between food intake in the first ten days of the experiment and gestation period, fasting blood sugar (FBS), TG, and homeostatic model assessment (HOMA) index. Moreover, asprosin levels had a significant and negative correlation with HDL and insulin levels. Results showed, synbiotic supplementation has beneficial effects on obese animals and improves weight gain during pregnancy, pup birth weight, FBS, insulin resistance and lipid profile. These advantages of synbiotic supplementation could be mediated by reducing serum asprosin levels.

The relationship of serum asprosin level with diabetic and non-diabetic retinopathy.

This study was aimed at investigating the role of serum asprosin level in diabetic retinopathy pathogenesis and differential diagnosis diabetic and non-diabetic retinopathy. The cross-sectional study was conducted between May 2021 and August 2021. A total of 21 subjects with diabetic retinopathy, 21 subjects with non-diabetic retinopathy, 21 subjects with type 2 diabetes mellitus (T2DM) without retinopathy and 21 healthy controls were included in the study. Biochemical parameters, serum asprosin, serum IL-6 and TNF-α levels were measured in all participants. Fasting blood glucose (FBG), HbA1c, HOMA-IR and LDL levels were higher in diabetic patients than non-diabetic. The blood asprosin levels were higher in the diabetic retinopathy group compared to the healthy control group (p=0.001), T2DM without diabetic retinopathy (p=0.010), and non-diabetic retinopathy group (p=0.043). There is a significant positive relationship between asprosin level and high FBG, HbA1c and HOMA-IR scores. Serum asprosin level is significantly increased in DRP group than others. A high asprosin level might be a risk factor for the development of diabetic complications, such as diabetic retinopathy. These findings suggest that the measurement of serum asprosin level may support clinicians in determining the risk of DRP development.

Association of maternal and umbilical cord blood asprosin with excessive gestational weight gain.

Maternal obesity and excessive gestational weight gain (EGWG) may have persistent effects on offspring obesity and be risk factors for both mother and child. Studies have reported that asprosin concentration is associated with metabolism and weight changes during pregnancy. This study therefore evaluated the association of maternal and newborn asprosin with normal weight gain and EGWG and nutritional intake in pregnancy. The study included 30 pregnant women with normal weight gain and 30 women with EGWG referred to Ali ibn Abi Talib Hospital in Zahedan, Iran, September 2020 to June 2021. A demographic questionnaire and neonatal complications checklist were completed. Asprosin concentrations at the time of delivery in maternal venous blood samples and umbilical vein blood samples were measured by ELISA technique. Macronutrient and energy intake were assessed by a 24-h dietary recall questionnaire and compared with standard Recommended Dietary Allowance (RDA) and Dietary References Intake (DRI) values. Asprosin levels were significantly higher in the EGWG group's umbilical cord blood than in the control group but there was no difference in maternal asprosin concentrations between the two groups. The Appearance, Pulse, Grimace, Activity and Respiration (Apgar) score was significantly lower in the EGWG group than in the control group, although there was no difference in birthweight between the groups. Weight gain during pregnancy,energy intake and protein and carbohydrate consumption were significantly higher inthe EGWG group than in the control group (p<0.05). It seems that differences in asprosin secretion do not mediate an imbalance in energy intake and other macronutrients during pregnancy that affect pregnancy weight gain and birthweight. However, excessive gestational weight gain was associated with neonatal asprosin levels and newborn Apgar scores.

Asprosin induces vascular endothelial-to-mesenchymal transition in diabetic lower extremity peripheral artery disease

BackgroundAltered adipokine secretion in dysfunctional adipose tissue facilitates the development of atherosclerotic diseases including lower extremity peripheral artery disease (PAD). Asprosin is a recently identified adipokine and displays potent regulatory role in metabolism, but the relationship between asprosin and lower extremity PAD remains uninvestigated.Methods33 type 2 diabetes mellitus (T2DM) patients (DM), 51 T2DM patients with PAD (DM + PAD) and 30 healthy normal control (NC) volunteers were recruited and the blood samples were collected for detecting the circulatory asprosin level and metabolomic screening. RNA sequencing was performed using the aorta tissues from the type 2 diabetic db/db mice and human umbilical vein endothelial cells (HUVECs) were treated with asprosin to determine its impact on the endothelial-to-mesenchymal transition (EndMT).ResultsThe circulating levels of asprosin in DM + PAD group were significantly higher than that of NC group and the DM group. Circulating asprosin level was remarkably negatively correlated with ankle-brachial index (ABI), even after adjusting for age, sex, body mass index (BMI) and other traditional risk factors of PAD. Logistic regression analysis revealed that asprosin is an independent risk factor for PAD and receiver-operator characteristic (ROC) curve determined a good sensitivity (74.5%) and specificity (74.6%) of asprosin to distinguish PAD. Data from metabolomics displayed a typical characteristics of de novo amino acid synthesis in collagen protein production by myofibroblasts in patients with PAD and activation of TGF-β signaling pathway appeared in the aortic tissue of db/db mice. Asprosin directly induces EndMT in HUVECs in a TGF-β-dependent manner as TGF-β signaling pathway inhibitor SB431542 erased the promotional effect of asprosin on EndMT.ConclusionsElevated circulatory asprosin level is an independent risk factor of lower extremity PAD and might serve as a diagnostic marker. Mechanistically, asprosin directly induces EndMT that participates in vascular injury via activation of TGF-β signaling pathway.Trial registration This trial was registered at clinicaltrials.gov as NCT05068895

Correlation of metabolic characteristics with maternal, fetal and placental asprosin in human pregnancy

ObjectiveAsprosin is a recently discovered hormone associated with obesity and diabetes mellitus. Little is known about asprosin’s role during pregnancy, but a contribution of asprosin to pregnancy complications resulting from maternal obesity and gestational diabetes mellitus (GDM) is conceivable. We assessed the potential effects of obesity, GDM and other clinical parameters on maternal and fetal umbilical plasma asprosin concentrations and placental asprosin expression.DesignThe Cologne-Placenta Cohort Study comprises 247 female patients, from whom blood and placentas were collected at the University Hospital Cologne.MethodsWe studied the maternal and fetal umbilical plasma and placentas of pregnant women with an elective, primary section. Sandwich ELISA measurements of maternal and fetal umbilical plasma and immunohistochemical stainings of placental tissue were performed to determine the asprosin levels. Also, the relation between asprosin levels and clinical blood parameters was studied.ResultsThere was a strong correlation between the maternal and fetal plasma asprosin levels and both increased with GDM in normal-weight and obese women. Asprosin immunoreactivity was measured in cultivated placental cells and placental tissue. BMI and GDM were not but pre-pregnancy exercise and smoking were correlated with maternal and/or fetal asprosin levels. Placental asprosin levels were associated with maternal but not with fetal plasma asprosin levels and with BMI but not with GDM. Placental asprosin was related to maternal insulin levels and increased upon insulin treatment in GDM patients.ConclusionsAsprosin could potentially act as a biomarker and contribute to the clinical manifestation of pregnancy complications associated with maternal obesity.

Laboratory evidence on a direct correlation between acute central serous chorioretinopathy and tenascin C, metalloprotein 1, BAX, BCL2, subfatin and asprosin

Central serous chorioretinopathy (CSCR) is an eye disease of unknown etiology that presents with reduced visual acuity, choroidal thickening (distance between Bruch's membrane and the chorioscleral border), and subretinal fluid leakage. In the present study, the goal was to investigate the role of the interrelated tenascin C, metalloprotein-1, BAX, BCL2, subfatin and asprosin molecules in the pathogenesis of CSCR. Thirty CSCR patients and 30 controls were included. CSCR was diagnosed by optical coherence tomography imaging. A 5mL blood sample was collected from all participants after overnight fasting. Compounds in the blood samples were studied with the Enzyme-Linked Immunosorbent Assay (ELISA) method. Patients with CSCR were found to have macular thickening (P: 0.08) and statistically significantly reduced visual acuity (P: 0.034) compared to controls. With regard to serum parameters, there were statistically significant increases in tenascin C, metalloprotein-1, BAX, BCL2, subfatin and asprosin levels compared to controls. We found a positive correlation between macular thickness and tenascin C (r+0.670, P<0.001), metaloprotein-1 (r+0.714, P<0.001), BAX, BCL2 (r+0.771, P<0.001), subfatin and asprosin levels and a negative correlation between visual acuity and tenascin C (r+0.605 P<0.001), metaloprotein-1 (r+0.704, P<0.001), BAX, BCL2 (r+0.738, P<0.001), subfatin and asprosin levels. The molecules studied herein were negatively correlated with visual acuity and positively correlated with macular thickness, suggesting that these molecules might have a role in the pathogenesis of CSCR. Thus, we predict that these molecules could be new candidates for the diagnosis and follow-up of CSCR in the future.

Sensitive asprosin detection in clinical samples reveals serum/saliva correlation and indicates cartilage as source for serum asprosin

The C-terminal pro-fibrillin-1 propeptide asprosin is described as white adipose tissue derived hormone that stimulates rapid hepatic glucose release and activates hunger-promoting hypothalamic neurons. Numerous studies proposed correlations of asprosin levels with clinical parameters. However, the enormous variability of reported serum and plasma asprosin levels illustrates the need for sensitive and reliable detection methods in clinical samples. Here we report on newly developed biochemical methods for asprosin concentration and detection in several body fluids including serum, plasma, saliva, breast milk, and urine. Since we found that glycosylation impacts human asprosin detection we analyzed its glycosylation profile. Employing a new sandwich ELISA revealed that serum and saliva asprosin correlate strongly, depend on biological sex, and feeding status. To investigate the contribution of connective tissue-derived asprosin to serum levels we screened two cohorts with described cartilage turnover. Serum asprosin correlated with COMP, a marker for cartilage degradation upon running exercise and after total hip replacement surgery. This together with our finding that asprosin is produced by primary human chondrocytes and expressed in human cartilage suggests a contribution of cartilage to serum asprosin. Furthermore, we determined asprosin levels in breast milk, and urine, for the first time, and propose saliva asprosin as an accessible clinical marker for future studies.

The relationship of asprosin with β-hydroxybutyric acid and postpartum disorders in cows.

The aim of the present study was to determine asprosin levels in cows, the relationship of this hormone with postpartum disorders and β-hydroxybutyric acid, and also the potential of asprosin to be a marker for postpartum diseases. The study was designed as a two-stage trial. In the first stage, blood asprosin and β-hydroxybutyric acid levels of 20 healthy Simmental cows aged 3-4 years were measured at the time of calving, and on days 3, 6, 9, 12 and 15 postpartum. In the second stage, 200 cows were divided into two groups: (1) healthy (n = 100) and (2) diseased (placental retention, hypocalcaemia, metritis, lameness, abomasal displacement, mastitis; n = 100); asprosin and β-hydroxybutyric acid concentrations of the blood were assessed on day 15 postpartum. In conclusion, the asprosin level was found to be at measurable levels in cows, and a negative correlation with β-hydroxybutyric acid was found. According to these findings, the data obtained from this study could be used for the prevention, control and treatment of some postpartum disorders associated with ketosis and for developing novel hypotheses concerning the actions of this hormone. It was concluded that further studies are required to reveal the associations between asprosin and postpartum disorders.

Evaluation of serum levels of asprosin and other metabolic profiles in patients with idiopathic tonic-clonic generalized epilepsy on treatment with valproic acid.

This cross-sectional research was undertaken to determine the serum levels of asprosin, a novel white adipose tissue-derived glucogenic adipokine, in epileptic patients on valproic acid treatment. Sixty-six patients diagnosed with idiopathic tonic-clonic generalized epilepsy were divided into three groups: those treated with valproic acid (n = 22), those treated with lamotrigine (n = 22), and twenty-two newly diagnosed or untreated patients. A control group was twenty-two, healthy volunteers with a similar distribution of gender and age. Body mass index (BMI) and fasting serum levels of asprosin, glucose, glycohemoglobin(HbA1c), insulin, and lipid profile were measured for both patients and control groups. Additionally, homeostasis model assessment for insulin resistance (HOMA-IR) was also calculated for the investigated groups. The mean BMI values and fasting serum levels of glucose, HbA1c, insulin, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglyceride were much higher in subjects treated with valproic acid than those in the other study groups. Furthermore, a higher number of participants in the valproic acid group fulfilled the insulin resistance criterion (defined as HOMA-IR > 2.5) compared with those in other study groups. The mean fasting serum asprosin concentration was also significantly higher in the valproic acid group than in otherstudy groups. This was while the values of the study parameters were comparable in the healthy, un-treated, and lamotrigine groups. Our finding suggested that elevated asprosin level might be one of the pathological mechanisms involved in the development of obesity, insulin resistance, and metabolic disturbances related to valproic acid treatment.

Meal-Related Asprosin Serum Levels Are Affected by Insulin Resistance and Impaired Fasting Glucose in Children With Obesity.

Asprosin physiologically increases in fasting conditions and decreases with refeeding and has been implicated in glucose homeostasis. An alteration of meal-related circadian oscillation of asprosin has been suggested in adults affected by type 2 diabetes mellitus.Aims of this study were to test the hypothesis of an alteration in the meal-related variation of asprosin levels in non-diabetic children and adolescents with obesity and to assess which metabolic variables condition this variation in non-diabetic children and adolescents with obesity. This is a cross-sectional study which included 79 children and adolescents with obesity. Children underwent clinical and biochemical assessments, including oral glucose tolerance test (OGTT), and liver ultrasound evaluation. Asprosin serum levels were measured by an enzyme-linked immunosorbent assay at a fasting state and at the 120-minute OGTT timepoint (2h-postprandial asprosin). Fasting and 2h-postprandial asprosin serum levels did not significantly differ in the entire study population (374.28 ± 77.23 vs 375.27 ± 81.26;p=0.837). 55.7% of patients had a significant increase in 2h-postprandial asprosin compared with fasting levels. The asprosin level increase condition was significantly associated with HOMA-IR (OR,1.41; 95%CI,1.005-1.977; p=0.047), fasting glycaemia (OR,1.073; 95%CI,1.009-1.141;p=0.024) and HOMA-B (OR,0.99; 95%CI,0.984-0.999; p=0.035). Moreover, the IFG condition was associated with the increase in asprosin levels (OR, 3.040; 95%CI, 1.095-8.436; p=0.033), even after adjustment for HOMA-IR, BMI SDS, sex and pubertal stage. Insulin resistance and IFG influence meal-related changes of asprosin serum levels in our study population of obese, non-diabetic, children. Alteration of asprosin circadian secretion might be an early biomarker of impaired glucose regulation in obese children with insulin resistance.

Sex-Specific Effects of Maternal and Post-Weaning High-Fat Diet on Adipose Tissue Remodeling and Asprosin Expression in Mice Offspring.

Perinatal high-fat diet (HFD) increases risk of metabolic disorders in offspring. Adipose tissue remodeling is associated with metabolic syndrome. The current study characterizes the profile of maternal HFD-induced changes in adipose tissue remodeling and adipokines expression in mice offspring. Female C57BL/6 mice are fed with CHOW or HFD for 2 weeks before mating, throughout gestation and lactation. At weaning, pups are randomly fed with CHOW or HFD, resulting in eight groups according to sex and maternal diet: Male CHOW-CHOW (MCC), Male CHOW-HFD (MCH), Male HFD-CHOW (MHC), Male HFD-HFD (MHH), Female CHOW-CHOW (FCC), Female CHOW-HFD (FCH), Female HFD-CHOW (FHC), and Female HFD-HFD (FHH). Increased body weight, impaired glucose tolerance, increased adipose tissue mass and hypertrophy, and decreased circulating asprosin level are only observed in male offspring exposure to maternal HFD. Serum asprosin level negatively correlates with fasting blood glucose, serum cholesterol (CHO), and high-density lipoprotein (HDL) levels, while positively correlates with serum low-density lipoprotein (LDL) and glutamate-oxaloacetate transaminase (GOT) levels in male offspring. A combination of genetic and biochemical analyses of adipokines shows the depot- and sex-specific changes in response to maternal and/or post-weaning HFD. This study's results reveal the differential metabolic changes in response to maternal and/or post-weaning HFD in male and female offspring. The effect of maternal HFD on metabolic phonotype is more obvious in male offspring, supporting the notion that males are more susceptible to HFD-induced metabolic disorders.

Two Important Players for Type 2 Diabetes Mellitus: Metrnl and Asprosin.

The prevalence of diabetes mellitus (DM) is rapidly increasing worldwide. Metrnl and asprosin are the new adipomyokins that can increase glucose tolerance and affect insulin resistance. Based on this information, we aimed to identify the possible relationship between T2DM and asprosin, Metrnl levels and insulin resistance. Our study consisted of a group of 60 patients (female: 30/male: 30) who were newly diagnosed with T2DM and did not take any medications and a control group of 60 healthy (female: 31 - male: 29) individuals. We found that serum Metrnl levels were significantly lower in the diabetic group than in the control group (p < 0.01). In contrast, serum asprosin levels were significantly higher in the diabetic group compared to the control group (p < 0.01). We found a positive correlation between asprosin levels and HOMA-IR, insulin, BMI, and triglyceride levels in the patient group. On the contrary, we found a negative correlation between Metrnl levels and HOMA-IR, insulin, triglyceride, glucose levels. In the literature review, we could not find a comparison study on the relationship between T2DM, Metrnl, asprosin levels, and HOMA-IR in humans. As far as we know, this study will be the first report in which both adipokine/adipomyokine are compared and associated with HOMA-IR. Asprosin levels in patients with T2DM are higher than healthy people, and Metrnl levels are lower. These two molecules (Metrnl and asprosin) have the ability to be an early warning signal of insulin resistance for T2DM.

Investigation of serum asprosin level in patients diagnosed of polycystic ovary syndrome in adolescent age

Polycystic ovary syndrome characterized by irregular menstruation, high serum androgen levels and infertility in the reproductive period. New markers are being studied to facilitate diagnosis. Asprosin is a peptide that is synthesized during fasting and stimulates glucose production from the liver. High levels of asprosin have been found to be associated with obesity, insulin resistance and diabetes. The aim is to answer the question 'Can serum asprosin level be used as a marker in the initial diagnosis of PCOS in adolescents without any disease?'. A total of 65 people between the ages of 12-18 who applied to the Antalya Training and Research Hospital Gynecology and Obstetrics Polyclinic between June 2020 and January 2021 were included in the study. The group was divided into two as 38 patients newly diagnosed with PCOS and 27 healthy control groups without any pathology. When the asprosin level of the cases diagnosed with PCOS and the cases in the control group were compared, it was observed that the asprosin level of the cases with PCOS was significantly higher (p=0.004). This study was a study showing that serum asprosin level can be used in the diagnosis of PCOS. It should be supported by other studies.

Asprosin and Oxidative Stress Level in COVID-19 Patients.

The global COVID-19 pandemic, caused by the SARS-CoV-2 virus, has created great problems in healthcare systems throughout the world. Although, just like other respiratory tract viral infections, it is a disease with pathophysiological processes associated in general with cytokine production, inflammation, cell death, and redox imbalance or oxidative stress, very little is known about the pathology. Also, in recent studies, the effect of asprosin, which has an important and complex role on metabolism, on COVID-19 is unknown. The aim of this study is to determine the level of asprosin, a new hormone that has the potential to affect many metabolic pathways such as glucose metabolism, in COVID-19 patients. In addition, it is to determine whether asprosin is associated with oxidative stress in COVID-19 patients. Blood samples were taken from 30 patients diagnosed with COVID-19 confirmed with RT-PCR test and 30 healthy control subjects. The serum asprosin level was analyzed with ELISA, and total antioxidant status (TAS) and total oxidant status (TOS) levels with colorimetric analysis. The asprosin and TAS levels were determined to be statistically significantly decreased in the COVID-19 patients, and the TOS and OSI levels were significantly increased. It can be thought that a decrease in asprosin level in COVID-19 patients causes a decrease in metabolic activity, prevents sufficient energy production in patients, and therefore oxidative stress increases in patients.

Evaluation of Plasma Asprosin Concentration in Patients with Coronary Artery Disease.

IntroductionThe goal of this study is to investigate the association between diagnosis and severity of coronary artery disease (CAD) and Asprosin level.MethodsPatients diagnosed with CAD who underwent conventional coronary angiography for the first time were included in the present study. The patients were divided into four groups, each consisting of 20 individuals, as medical group, single coronary lesion group, double coronary lesion group, and multiple coronary lesions group. Serum Asprosin values and Gensini scores of the groups were compared in terms of compliance.ResultsIn this study, Asprosin values were found to be significantly higher in the multiple coronary lesions group than in the medical, single coronary, and double coronary lesion groups (P<0.05). In the double coronary lesion group, Asprosin values were significantly higher (P<0.05) than the in the medical and single coronary lesion groups. It was also found that Asprosin values did not differ at significant levels in the medical and single coronary lesion groups (P>0.05). It was determined that the increases in Asprosin values and Gensini scores were compatible with each other.ConclusionThe present study showed that the increases in serum Asprosin levels, along with the increases in the number of coronary arteries with critical stenosis, might be a marker in diagnosing and determining the severity of CAD.

Serum asprosin levels are associated with obesity and insulin resistance in Arab adults

BackgroundAsprosin, a novel adipokine, has been implicated in glucose regulation, insulin production, and appetite stimulation. Hence, the current study explores circulating asprosin levels and their associations with insulin resistance (IR) and other parameters in obese and type 2 diabetes mellitus (T2DM) Saudi subjects. MethodsA total of N = 291 (89 control, 105 T2DM/obese and 97 obese) subjects were included in this cross-sectional study. Fasting glucose and lipid profiles were measured routinely. Adiponectin, leptin, C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1, and asprosin were measured using commercially available assays. ResultsSerum asprosin levels were found to be significantly highest in obese subjects [3.7 ng/ml (2.6–5.0)] than T2DM/obese [0.1 ng/ml (0.0–0.4)] and controls [0.2 ng/ml (0.1–0.3)] (p < 0.001). In the T2DM/obese group, users of metformin alone or in combination had significantly lower asprosin levels than those whose medication history was unknown [0.03 ng/ml (0.02–0.05) versus 0.2 ng/ml (0.1–0.4); p < 0.001]. Stepwise multiple linear regression analysis revealed that only glucose, insulin and adiponectin were the most important predictors of asprosin, explaining 61.3% (p < 0.001) of the variances perceived. ConclusionAsprosin levels are associated with markers of IR independent of adiposity and inflammation and are influenced by oral hypoglycemics, particularly metformin.

A Serum Marker for Early Pancreatic Cancer With a Possible Link to Diabetes.

Pancreatic cancer (PC) has a grim prognosis, and an early diagnostic biomarker has been highly desired. The molecular link between diabetes and PC has not been well established. Bioinformatics screening was performed for a serum PC marker. Experiments in cell lines (5 PC and 1 normal cell lines), mouse models, and human tissue staining (37 PC and 10 normal cases) were performed to test asprosin production from PC. Asprosin's diagnostic performance was tested with serums from multi-center cohorts (347 PC, 209 normal, and 55 additional diabetic patients) and evaluated according to PC status, stages, and diabetic status, which was compared with that of CA19-9. Asprosin, a diabetes-related hormone, was found from the bioinformatics screening, and its production from PC was confirmed. Serum asprosin levels from multi-center cohorts yielded an age-adjusted diagnostic area under the curve (AUC) of 0.987 (95% confidence interval [CI] = 0.961 to 0.997), superior to that of CA19-9 (AUC = 0.876, 95% CI = 0.847 to 0.905), and a cut-off of 7.18 ng/mL, at which the validation set exhibited a sensitivity of 0.957 and a specificity of 0.924. Importantly, the performance was maintained in early-stage and non-metastatic PC, consistent with the tissue staining. A slightly lower performance against additional diabetic patients (n = 55) was restored by combining asprosin and CA19-9 (AUC = 0.985, 95% CI = 0.975 to 0.995). Asprosin is presented as an early-stage PC serum marker that may provide clues for PC-induced diabetes. Larger prospective clinical studies are warranted to solidify its utility.

CYP1A2 polymorphisms modify the association of habitual coffee consumption with appetite, macronutrient intake, and body mass index: results from an observational cohort and a cross-over randomized study.

Evidence regarding the influence of coffee on appetite and weight control is equivocal and the influence of covariates, such as genetic variation in caffeine metabolism, remains unknown. Herein, we addressed the novel hypothesis that genetic variation in CYP1A2, a gene responsible for more than 95% of caffeine metabolism, differentially impacts the association of coffee consumption with appetite and BMI among individuals with different genetic predispositions to obesity. A cross-over randomized intervention study involving 18 volunteers assessed the effects of coffee consumption on dietary intake, appetite, and levels of the appetite-controlling hormones asprosin and leptin. Data on habitual coffee intake, BMI, and perceived appetite were obtained from an observational cohort of 284 volunteers using validated questionnaires. Participants were stratified according to a validated genetic risk score (GRS) for obesity and to the -163C > A (rs762551) polymorphism of CYP1A2 as rapid (AA), intermediate (AC), or slow (CC) caffeine metabolizers. Coffee consumption led to lower energy and dietary fat intake and circulating asprosin levels (P for interaction of rs762551 genotype*coffee consumption=0.056, 0.039, and 0.043, respectively) as compared to slow/intermediate metabolizers. High coffee consumption was more prevalent in rapid compared to slow metabolizers (P = 0.008 after adjustment for age, sex, and BMI) and was associated with lower appetite perception and lower BMI only in rapid metabolizers (P for interaction of rs762551 genotype*coffee consumption = 0.002 and 0.048, respectively). This differential association of rs762551 genotype and coffee consumption with BMI was more evident in individuals at higher genetic risk of obesity (mean adjusted difference in BMI = -5.82 kg/m2 for rapid versus slow/intermediate metabolizers who consumed more than 14 cups of coffee per week). CYP1A2 rs762551 polymorphism modifies the association of habitual coffee consumption with BMI, in part by influencing appetite, energy intake and circulating levels of the orexigenic hormone asprosin. This association is more evident in subjects with high genetic predisposition to obesity. ClinicalTrials.gov: registered Clinical Trial NCT04514588.

Serum levels of Asprosin in patients diagnosed with coronary artery disease (CAD): a case-control study

BackgroundCoronary artery disease (CAD) is considered as a multi-faceted chronic inflammatory disease involving reduced blood supply to the myocardium as a result of accumulating lipids in the atrial walls. Visceral adiposity with disrupted release of adipokines play a key role in its pathogenesis. Asprosin is a newly identified fasting-induced glucogenic adipokine that has been related with metabolic disorders such as type II diabetes mellitus and polycystic ovary syndrome. The preset study sought to assess circulating asprosin in context of CAD.MethodsIn this study, serum levels of asprosin were determined in 88 CAD patients and 88 non-CAD healthy controls. Serum IL-6, TNF-α, asprosin and adiponectin were assessed using ELISA kits.Results: Serum asprosin was found to be higher in CAD patients when compared to non-CAD subjects (7.84 ± 2.08 versus 5.02 ± 1.29 μg/mL, p < 0.001). Similarly, serum TNF-α, and IL-6 elevated in CAD group significantly (p < 0.001). However, circulating adiponectin diminished in CAD group when compared with non-CAD subjects (p < 0.001). Moreover, serum asprosin levels directly correlated with BMI, FBG, HOMA-IR, TG and TC. Logistic regression analyses showed that asprosin levels were associated with increased risk of developing CAD (odds ratio: 3.01, 95% CI: 2.16, 4.20 and p < 0.001), after adjusting for potential confounders (age, sex and BMI).ConclusionsThe present study findings suggested a possible relation of serum asprosin with the pathogenesis of CAD, in particular through insulin resistance and dyslipidemia.

A pancancer overview of FBN1, asprosin and its cognate receptor OR4M1 with detailed expression profiling in ovarian cancer.

Ovarian cancer affects >295,000 women worldwide and is the most lethal of gynaecological malignancies. Often diagnosed at a late stage, current research efforts seek to further the molecular understanding of its aetiopathogenesis and the development of novel biomarkers. The present study investigated the expression levels of the glucogenic hormone asprosin [encoded by fibrillin-1 (FBN1)], and its cognate receptor, olfactory receptor 4M1 (OR4M1), in ovarian cancer. A blend of in silico open access The Cancer Genome Atlas data, as well as in vitro reverse transcription-quantitative PCR (RT-qPCR), immunohistochemistry and immunofluorescence data were used. RT-qPCR revealed expression levels of OR4M1 and FBN1 in clinical samples and in ovarian cancer cell lines (SKOV-3, PEO1, PEO4 and MDAH-2774), as well as the normal human ovarian surface epithelial cell line (HOSEpiC). Immunohistochemical staining of a tissue microarray was used to identify the expression levels of OR4M1 and asprosin in ovarian cancer samples of varying histological subtype and grade, including clear cell carcinoma, serous ovarian cancer and mucinous adenocarcinoma. Immunofluorescence analysis revealed asprosin expression in SKOV-3 and HOSEpiC cells. These results demonstrated the expression of both asprosin and OR4M1 in normal and malignant human ovarian tissues. This research invokes further investigation to advance the understanding of the role of asprosin and OR4M1 within the ovarian tumour microenvironment.