Plasma and aqueous levels of subfatin, preptin and betatrophin in patients with diabetic retinopathy.

AIM: To examine subfatin, preptin and betatrophin levels in plasma and aqueous in patients with diabetes mellitus (DM) (with and without retinopathy). MATERIAL AND METHOD: Sixty patients, who were similar in terms of age and gender, and were scheduled for operation due to cataract, were included in the study. The patients were divided into three groups as Group C (20 weeks without diabetes and comorbidity), Group DM (20 patients with DM but no retinopathy) and Group DR (20 patients with diabetic retinopathy). The preoperative body mass index (BMI), fasting plasma glucose, HbA1c, lipid profile levels of all patients in the groups were examined. Blood samples were also taken for plasma subfatin, preptin and betatrophin levels. At the beginning of the cataract surgery, 0.1 ml of aqueous fluid was taken from the anterior chamber. Plasma and aqueous subfatin, preptin and betatrophin levels were analyzed by ELISA (enzyme-linked immunosorbent assays) method. RESULTS: In our study results, there was a significant difference in BMI, fasting plasma glucose and hemoglobin A1c levels (p < 0.05 for all parameters). Plasma and aqueous subfatin levels were higher in Group DR compared to Group C (p < 0.001, p = 0.036, respectively). Plasma and aqueous preptin levels were higher in group DR and group DM than in group C (p = 0.001, p = 0.002, p < 0.001, p = 0.001, respectively). Plasma and aqueous betatrophin levels were higher in Group DR compared to group C (p = 0.001, p = 0.010, respectively). CONCLUSION: Subfatin, preptin and betatrophin molecules may have an important role in the pathogenesis of diabetic retinopathy.

Potential emerging roles of the novel adipokines adipolin/CTRP12 and meteorin-like/METRNL in obesity-osteoarthritis interplay.

BACKGROUND: Several insights into obesity-osteoarthritis (OA) relationship have been recently highlighted. Adipolin and metrnl are new adipokines also secreted by chondrocytes. However, their role in OA, and obesity-OA interplay hasn't been elucidated. Therefore, this study was designed to investigate the circulating as well as synovial fluid (SF) levels of adipolin and metrnl in osteoarthritic-patients compared to non-osteoarthritic subjects, and to study their association with OA-severity, dyslipidemia and insulin resistance (IR). METHODS: Patients with osteoarthritis and obesity (n = 30), and subjects with obesity not suffering OA (n = 25) were enrolled in the current study. Circulating and SF-levels of adipolin, metrnl, and insulin, as well as SF-levels of matrix-metalloproteinase-13 (MMP-13) were measured by ELISA. Knee-radiographs using X-ray were done to determine OA-severity, and investigate its association with adipokines' levels. RESULTS: Serum and SF-adipolin levels showed tendency to be lower in OA-patients compared to non-OA-subjects; serum: 0.64 [0.45-0.85] and 0.73 [0.62-0.78] ng/ml, p = 0.174, and SF: 0.53 [0.34-0.69] and 0.63 [0.44-0.74] ng/ml, p = 0.353, respectively. Additionally, serum adipolin showed negative-association with SF-MMP-13. However, when stratifying OA-patients into various severity grades, serum adipolin levels did not show a significant difference between them. Regarding serum metrnl, it was significantly lower in OA-patients compared to non-OA-subjects; 19.68 [10.40-53.40] and 48.83 [20.80-86.60] pg/ml, respectively, p = 0.018. Surprisingly, SF-metrnl levels were higher in OA-patients compared to non-OA-subjects; 912 [367-1524] and 315 [125-484] pg/ml, respectively, p = 0.007. SF-metrnl showed positive-association with insulin resistance, and negative-association with SF-MMP-13. Moreover, higher serum metrnl levels were found to be slightly associated with lower likelihood of OA in subjects with obesity; OR = 0.978, CI (0.960- 0.996), p = 0.02, and its levels were also found to be relatively lower in grade-4 compared to the less severe OAgrades. CONCLUSIONS: Metrnl, and to a lesser extent adipolin seem to be interrelated with OA. Different in-context regulatory mechanisms for metrnl production from various tissues are strongly suggested. Importantly, the findings of the current study shed lights on metrnl as a potential novel mediator and therapeutic target to consider in obesity-OA interplay.

The blooming intersection of subfatin and metabolic syndrome.

Metabolic Syndrome (MS) remains the leading cause of mortality and morbidity globally. Adipose tissue releases adipokines that play key roles in metabolic and cardio-cerebro-vascular homeostasis. Subfatin, induced after exercise or upon cold exposure in adipose tissue, is a novel secreted protein homologous to Metrn, a neutrophic factor with angiogenic properties. The protein was proved to be of great significance in the browning of white adipose tissue (BWT) and insulin resistance (IR). It affected insulin sensitivity at least via its local autocrine/paracrine action through AMP-activated protein kinase (AMPK) or peroxisome proliferator-activated receptor δ (PPAR-δ) dependent signaling. Subfatin blocked the release of inflammatory mediators, improved intracellular insulin signal transduction and reversed IR. It also improved glucose tolerance and played a key role in metabolism and cardiovascular and cerebrovascular homeostasis. It was reported that the level of serum subfatin was significantly correlated with the occurrence and severity of coronary heart disease, which might be a new target for the treatment of coronary heart disease. In addition, exercise increased the level of subfatin in circulation and adipose tissue, promoted energy consumption, improved glucose and lipid metabolism, increased the heat production of brown fat, and strengthened the anti-inflammatory mechanism. Given its role in metabolic disorders, subfatin is considered as a candidate biomarker of MS. However, the clinical significance of subfatin remains largely unclear. The purpose of this article is to review the research on the effect of subfatin on MS in recent years.

Subfatin and asprosin, two new metabolic players of polycystic ovary syndrome.

Asprosin and subfatin are recently discovered two new hormones of adipocyte origin that play a role in the regulation of glucose metabolism. Polycystic ovary syndrome (PCOS) is a gynaecological syndrome presenting with energy turbulence. The aim of this study was to investigate whether asprosin and subfatin play a role in PCOS disease. Thirty participants with a diagnosis of PCOS and thirty control group participants were included in this case-control study. Hormone profiles of the participants (subfatin, asprosin, insulin, prolactin, thyroid-stimulating hormone (TSH), oestradiol (E2), follicle-stimulating hormone (FSH), luteinising hormone (LH), dehydroepiandrosterone sulphate (DHEA-SO4), lipid profiles [(total testosterone, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride, cholesterol)], fasting blood sugar (FBS) and high-sensitivity C-reactive protein (hs-CRP) values were measured. While the levels of asprosin, LDL and triglyceride, TSH, E2, FSH, LH, DHEA-SO4 were found to be significantly higher in patients with PCOS compared to controls (p = .005; p = .01), subfatin and HDL levels were found to be low. Significantly decreasing subfatin and increasing asprosin levels in circulation in PCOS may play a role in the etiopathology of this disease and that they may also be new candidate molecules in addition to classical laboratory parameters in the diagnosis and follow-up of PCOS in the future.Impact statementWhat is already known on this subject? The studies investigating the relationship between PCOS and asprosin are contradictory. Although subfatin has been studied in many metabolic diseases, it has not been studied yet whether it is associated with PCOS. Furthermore, whether there is a mutual relationship between subfatin and asprosin in patients with PCOS has not been studied yet.What do the results of this study add? This available data indicates that significantly decreasing subfatin and increasing asprosin levels in the circulation in PCOS may play a role in the etiopathology of this disease.What are the implications of these findings for clinical practice and/or further research? The findings are promising in that decreasing subfatin and increasing asprosin levels will shed new light on reproductive endocrinology changes caused by PCOS and may help to clarify the pathophysiology of PCOS. Furthermore, in our study, the asprosin/subfatin ratio was above three in PCOS disease. This ratio reported here is anticipated to contribute to the course or follow-up of the disease in the future. Also, subfatin has been investigated here for the first time, may also be a new candidate molecule in addition to classical laboratory parameters in the diagnosis and follow-up of PCOS.

The Plasma Levels of Protein Adiponectin (AdipoQ) and Meteorin-Like (Metrnl) in Newly Diagnosed Type 2 Diabetes Mellitus.

Purpose: This study aimed to measure the concentrations of the Adiponectin and Meteorin - Like (Metrnl) in newly diagnosed type 2 diabetes patients. Patients and Methods: A comparative cross-sectional study contained two groups: Group 1 (86 newly diagnosed diabetes mellitus type 2 patients) and group 2 (71 healthy persons). The plasma concentrations of Adiponectin and Metrnl were measured by Enzyme Link Immunosorbent Assay (ELISA). Results: The plasma level of Adiponectin of the newly diagnosed diabetes mellitus type 2 group and the healthy group were 1219.82 ng/mL (1132.43-2772.50) and 1187.25 ng/mL (1160.66-3807.50) respectively. The plasma level of Metrnl of two groups were 757.60 pg/mL (564.15-994.00) and 697.60 pg/mL (538.50-986.10) respectively. There were no significant difference between two groups. Metrnl had no correlation with glucose, HbA1c, lipid profile, BMI. Adiponectin had correlation with Metrnl and HDL-cholesterol. Adiponectin had no correlation to glucose, HbA1c, LDL-cholesterol, total cholesterol, triglyceride, BMI. People with the lower Adiponectin concentration had the higher risk of diabetes (OR=6.52; 95% CI: 2.43 -17.55). Conclusion: Adiponectin and Metrnl were not significantly different in newly diagnosed type 2 diabetes and healthy people. The lower concentration of Adiponectin might increase the risk of type 2 diabetes.

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

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.

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

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.

Subfatin, Asprosin, Alamandine and Maresin-1 Inflammation Molecules in Cardiopulmonary Bypass.

Purpose: Cardiopulmonary bypass (CPB) is a nonphysiological procedure in which inflammatory reactions and oxidative stress are induced, hormones and hemodynamic parameters are affected, and circulation is maintained outside the body. This study aimed to examine the effects of CPB on blood subfatin (SUB), asprossin (ASP), alamandine (ALA) and maresin-1 (MaR-1) levels. Materials and Methods: Controls and patients who underwent open-heart surgery with CPB and whose age and body mass indices were compatible with each other were included in the study. Venous blood samples were collected from CPB patients (n =19) before anesthesia induction (T1), before CPB (T2), 5 min before cross-clamp removal (T3), 5 min after cross-clamp removal (T4), when taken to the intensive care unit (T5), postoperative 24th hour (T6) and 72nd hour (T7) postoperatively. Venous blood was collected from the healthy controls (n =19). The amounts of SUB, ASP, ALA, and MaR-1 in the blood samples were measured using an Enzyme-Linked Immunosorbent Assay (ELISA). Results: The amounts of SUB and MaR-1 in the control group were significantly higher than those in CPB patients, while these parameters in T1-T3 blood gradually decreased in CPB patients (p<0.01). It was also reported that the amounts of ASP and ALA in the control group were significantly lower than those in CPB patients, whereas those parameters in the T1-T3 blood samples increased gradually in CPB patients, but started to decrease in T4-T7 blood samples. Conclusion: These hormonal changes in the organism due to CPB demonstrate that "hormonal metabolic adaptation" mechanisms may be activated to eliminate the negative consequences of surgery. According to these data, SUB, MaR-1, anti-alamandine, and anti-asprosin could be used in CPB surgeries may come to the fore in the future to increase the safety of CPB surgeries.

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

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.

Correlation of serum subfatin, cthrc1, ctrp3, ctrp6 levels with disease indices in patients with axial spondyloarthritis.

BACKGROUND: The study aimed to investigate novel biomarkers from the C1q TNF superfamily and evaluate their role in autoimmune inflammatory rheumatic diseases with the goal of identifying an effective biomarker to measure clinical disease activity and assess treatment efficacy. METHODS: Sixty-one Axial spondyloarthritis (AxSpa) patients and 30 healthy controls were enrolled in the study. The serum biomarkers subfatin, CTHRC1, CTRP3, CTRP6, IL-6, IL-17, and TNF-α and the disease indices BASDAI, BASFI, MASES, and ASDAS-ESR/CRP were evaluated and compared. The patients were then classified, and their serum biomarkers were assessed according to their ASDAS scores and their treatment regimens. RESULTS: Among the studied biomarkers, none showed a significant difference between the patients and the healthy controls. Although the difference was not statistically significant, the median values of serum subfatin, CTHRC1, CTRP3, CTRP6, IL-6, IL-17, and TNF-α were all found to be lower in the AxSpa patients than in the healthy controls. Furthermore, once the patients were classified regarding their disease activity, no correlation between the study biomarkers and levels of clinical disease indices was observed. Finally, biological treatments were found to affect the serum concentration of these biomarkers regardless of the level of disease activity. CONCLUSION: Novel adipokines and known modulators of inflammation, circulating subfatin, CTHRC1, CTRP3, CTRP6, IL-6, IL-17, and TNF-α levels may play a role in assessing treatment efficacy, especially in those treated with TNF-inhibitors. However, we failed to demonstrate a correlation between clinical disease activity and serum biomarker levels.

Subfatin concentration decreases in acute coronary syndrome.

Introduction: We investigated the association of serum subfatin concentration and acute myocardial infarction (AMI) in patients with ST-elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI). Materials and methods: In this study, patients who presented with chest pain (STEMI, NSTEMI, or non-cardiac chest pain) were included, i.e. 49 patients with non-cardiac chest pain (control) and 66 patients hospitalised with AMI. In the AMI group, 35 patients had NSTEMI and 31 had STEMI. Serum subfatin concentrations were determined via enzyme-linked immunosorbent assay (ELISA). Descriptive data on the patients and their comorbidities were recorded, and subfatin concentrations were analysed. Results: Subfatin concentrations were significantly different in the control, STEMI and NSTEMI groups (P = 0.002). In addition, subfatin concentrations were significantly lower in patients in the NSTEMI group than those in the control group (P < 0.001), but there was no significant difference between STEMI and the control group (P = 0.143). The receiver operating characteristic (ROC) analysis performed for differentiating the AMI and control groups found that subfatin had 64% sensitivity and 69% specificity, whereas troponin had 59% sensitivity and 95% specificity. In patients with AMI, the ROC analysis for differentiating NSTEMI from STEMI found that subfatin had 94% sensitivity and 41% specificity, while troponin had 65% sensitivity and 88% specificity. Conclusions: Subfatin concentrations were lower in patients without STEMI than in patients with STEMI. Subfatin concentration is associated with NSTEMI.

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

PURPOSE: 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. METHOD: 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. RESULTS: 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. CONCLUSION: 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.

Maternal and umbilical cord blood subfatin and spexin levels in patients with gestational diabetes mellitus.

Subfatin and spexin are two novel adipokines implicated in glucose homeostasis. This study was designed to investigate changes in blood subfatin and spexin levels during gestational diabetes mellitus (GDM) and childbirth, and define the mechanisms of these hormones in the physiopathology of GDM. A total of 60 pregnant women, comprising 30 diagnosed with GDM and 30 with normal gestation, were included in the study. The diagnosis of GDM was made through a 75-g oral glucose tolerance test (OGTT) administered between 24 and 28 weeks of pregnancy. The amounts of subfatin, spexin, and insulin were measured in blood samples by enzyme-linked immunosorbent assays; lipid profiles, glucose, and other biochemical parameters were measured by using an autoanalyzer. Levels of subfatin and spexin were significantly higher in blood samples drawn at baseline (before OGTT) in mothers with GDM compared to those with normal gestation. Similar observations were made in maternal and cord blood sampled at the end of pregnancy. However, at delivery, the increase in subfatin and spexin concentrations observed at baseline was abrogated in both groups of pregnant women, although levels in mothers with GDM were comparatively higher. These results show that levels of subfatin and spexin increased because of GDM and suggest that these hormones could be potential biomarkers for the diagnosis and management of GDM.

Serum levels of subfatin in patients with type 2 diabetes mellitus and its association with vascular adhesion molecules.

Subfatin is a newly discovered adipokine with insulin-sensitizing properties. Studies reported conflicting data with regard to the circulating levels and expression of Subfatin in the context of type 2 diabetes mellitus (T2DM) and obesity. The present study was conducted on 52 patients with T2DM, 36 prediabetes subjects, and 50 controls. The serum levels of Subfatin, adhesion molecules were measured by the ELISA technique. The serum Subfatin was lower in the T2DM and prediabetes groups. The serum levels of adhesion molecules were higher in the T2DM group. In addition, Subfatin demonstrated lower levels in obese patients with T2DM in comparison to lean T2DM patients. Furthermore, Subfatin showed a negative association with vascular adhesion molecules in prediabetes subjects and the T2DM group. A decrease in the serum Subfatin in T2DM patients and prediabetes subjects, and its association with vascular adhesion molecules suggested the possible role of Subfatin in diabetes and endothelial dysfunction.

Low serum levels of meteorin-like/subfatin: an indicator of diabetes mellitus and insulin resistance?

INTRODUCTION: Meteorin-like (Metrnl), also known as subfatin, is a recently discovered adipokine with a favourable effect on insulin sensitivity. Studies have shown lower Metrnl levels in obese patients. However, data on its circulating levels in type 2 diabetes mellitus (T2DM) patients are contradictory. This study aims to evaluate serum Metrnl levels in T2DM patients and determine the relationship between serum Metrnl levels and insulin resistance in these patients. MATERIAL AND METHODS: This cross-sectional study was conducted among 150 participants. The study was carried out between June 2019 and December 2019 at the internal medicine outpatient clinic of a tertiary university hospital. The participants were divided into three groups: group 1 (control group, n = 50), group 2 (newly diagnosed T2DM, n = 50), and group 3 (long-standing diagnosed T2DM, n = 50). An enzyme-linked immunosorbent assay (ELISA) was used to measure the serum levels of Subfatin (Metrnl), and the correlations of Metrnl level with anthropometric parameters, HOMA index, and biochemical measurements were assessed. RESULTS: There was no statistically significant difference between the gender (p = 0.468) and age (p = 0.067) characteristics of the three groups. The Metrnl (subfatin) levels of the participants were as follows: control group - 20.05 (1.56-103.78); newly diagnosed T2DM group - 2.62 (1.25-103.78); and long-standing diagnosed T2DM group - 2.01 (0.80-19.84) pg/mL. The Metrnl (subfatin) levels of the participants in the control group were higher than in the participants in the newly diagnosed T2DM and long-standing diagnosed T2DM groups (p < 0.001). Subfatin demonstrated a negative correlation with insulin and HOMA-IR in the control group and long-standing diagnosed T2DM group. CONCLUSIONS: The subfatin level was found to be higher in the healthy control group than in both diabetic patient groups. Subfatin level showed negative correlation with both insulin level and HOMA index. There was a relationship between subfatin and insulin resistance. Low levels of subfatin in the diabetic patient groups may play a role in the pathogenesis of T2DM by increasing insulin resistance.

Are maternal serum subfatin levels altered in women with one abnormal glucose tolerance test value?

SUMMARY BACKGROUND: Subfatin, a newly discovered adipokine, plays a pivotal role in the regulation of glucose metabolism. The relationship between gestational diabetes mellitus and maternal dyslipidemia is well-documented. AIMS: This study aims to assess serum subfatin levels and the triglyceride/high-density lipoprotein cholesterol ratio in women with one abnormal glucose tolerance test value and those with gestational diabetes mellitus. METHODS: In this case-control study, 105 pregnant women were categorized into three groups: women with normal 3-h oral glucose tolerance test results (n=35), women with one abnormal 3-h oral glucose tolerance test result (n=35), and women diagnosed with gestational diabetes mellitus (n=35). Serum subfatin levels were measured using human enzyme-linked immunosorbent assay kits. RESULTS: Serum subfatin levels were significantly lower in the gestational diabetes mellitus group (0.94±0.15 ng/mL) compared to the normal oral glucose tolerance test group (1.48±0.55 ng/mL) and the group with one abnormal oral glucose tolerance test result (1.50±0.59 ng/mL). The triglyceride/high-density lipoprotein cholesterol ratio was also lower in the healthy control group than in the gestational diabetes mellitus and one abnormal oral glucose tolerance test result groups. CONCLUSION: Serum subfatin levels in women with one abnormal abnormal glucose tolerance test value are compared to those in the control group, while the triglyceride/high-density lipoprotein cholesterol ratio is significantly altered in women with one abnormal abnormal glucose tolerance test value when compared to the control group.

Subfatin is a novel adipokine and unlike Meteorin in adipose and brain expression.

AIMS: Adipose tissue releases adipokines that play important roles in metabolic and cardio-cerebro-vascular homeostasis. This study was to discover novel adipokines using caloric restriction model. METHODS: Adipokine candidates were captured by gene array and bioinformatics analysis and verified by preparation of recombinant protein and antibody. RESULTS: We established a potential secreted protein database containing 208 genes and identified a novel adipokine, Subfatin, that was the highest expressed in subcutaneous fat of both rodents and humans among 15 detected tissues. The secreted mammalian Subfatin was a glycosylated protein. Subfatin was located diffusely throughout the adipose tissue except lipid droplets, with comparable expression between adipocytes and stromal cells, but much lower expression in macrophages than adipocytes. Subfatin was downregulated in white adipose tissue of caloric restriction rats, whereas dramatically upregulated during white adipocyte differentiation as well as in white adipose tissue of diet-induced obese mice. Subfatin was annotated as Meteorin-like (Metrnl) in public databases, a similar transcript of Meteorin (Metrn, also known as glial cell differentiation regulator). Meteorin displayed a brain-specific expression and was scarce in various adipose tissues, in contrast to the tissue expression patterns of Subfatin. CONCLUSIONS: Subfatin is a novel adipokine regulated by adipogenesis and obesity, with tissue distribution different from its homologue Meteorin.