Is there a relationship between serum vaspin levels and insulin resistance in chronic renal failure?

Objective: Chronic kidney disease [CKD] patients have insulin secretion disorders and resistance to insulin effects, that is responsible for the development of cardiovascular events. Vaspin is an adipocytokine that regulates glucose and lipid metabolism. We aimed to determine the serum vaspin levels and its relationship with insulin resistance in CKD patients

Methods: In the study groups, serum vaspin levels, anthropometric parameters and routine blood tests were measured. The serum vaspin levels were examined by the enzyme-linked immunosorbent assay [ELISA] and insulin resistance was determined by the homeostasis model assessment of insulin resistance [HOMA-IR] formula

Results: The serum vaspin, HOMA-IR index and insulin levels were observed significantly high in the CKD group in comparison with the control group. No correlation was found between the serum vaspin level and the anthropometric and metabolic values. The serum vaspin level was positively correlated with the fasting plasma glucose and age but without statistical significance

Conclusion: Insulin resistance and hyperinsulinemia contribute to the development of cardiovascular complications in CKD. We consider that the increase in the serum vaspin level is a consequence of the reduced renal excretion in the CKD and increases in response to insulin resistance

Follicular fluid cerebellin and betatrophin regulate the metabolic functions of growing follicles in polycystic ovary syndrome / 대한생식의학회지

OBJECTIVE: The aim of this study was to assess the changes of follicular fluid (FF) and serum levels of cerebellin precursor protein 1 (cbln1) and betatrophin in patients with polycystic ovary syndrome (PCOS) undergoing in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) with a gonadotropin-releasing hormone (GnRH) antagonist protocol. METHODS: Twenty infertile women with PCOS and 20 control women diagnosed as poor responders undergoing ovarian stimulation with a GnRH antagonist were included. Blood samples were obtained during ovum pick-up. Follicular fluid from a dominant follicle was collected from the subjects. Using enzyme-linked immunosorbent assays, FF and serum levels of cbln1 and betatrophin were measured in both groups of participants. Metabolic and hormonal parameters were also determined and correlated with each other. RESULTS: Both groups of women had similar serum and FF betatrophin levels (55.0±8.9 ng/mL vs. 53.1±10.3 ng/mL, p=0.11). The serum and FF betatrophin levels of poor responders were found to be similar (49.9±5.9 ng/mL vs. 48.9±10.7 ng/mL, p=0.22). Conversely, the FF cbln1 levels of PCOS women were found to be significantly higher than the serum cbln1 levels (589.1±147.6 ng/L vs. 531.7±74.3 ng/L, p<0.02). The FF cbln1 levels of control participants without PCOS were significantly higher than their serum cbln1 levels (599.3±211.5 ng/L vs. 525.3±87.0 ng/L, p=0.01). Positive correlations were detected among body mass index, insulin resistance, serum insulin, total testosterone, and betatrophin levels in the PCOS group. CONCLUSION: Follicular fluid betatrophin and cbln1 concentrations may play a pivotal role on follicular growth in PCOS subjects undergoing IVF/ICSI with an antagonist protocol.

investigation of tenascin-c levels in rheumatic mitral stenosis and their response to percutaneous mitral balloon valvuloplasty

The purpose of this study was to evaluate the tenascin-C levels in severe rheumatic mitral stenosis before and after percutaneous mitral balloon valvuloplasty [PMBV]. Forty patients with severe mitral stenosis requiring PMBV and 20 age-matched healthy subjects were included in the study. The mitral valve areas, mitral gradients and systolic pulmonary artery pressure [sPAP] were measured by echocardiography. The sPAP values and mitral gradients were also measured by catheterization before and after PMBV. The blood tenascin-C levels were measured before PMBV and 1 month after the procedure. The echocardiographic mean mitral gradients had a significant decrease after PMBV [11.7 +/- 2.8 vs. 5.6 +/- 1.7 mm Hg; p < 0.001] and also those of catheterization [13.9 +/- 4.4 vs. 4.0 +/- 2.4 mm Hg; p < 0.001]. Mitral valve areas increased significantly after PMBV [from 1.1 +/- 0.1 to 1.8 +/- 0.2 cm[2], p < 0.001]. Tenascin-C levels decreased significantly in patients after PMBV [from 15.0 +/- 3.8 to 10.9 +/- 3.1 ng/ml; p < 0.001]. Tenascin-C levels were higher in patients with mitral stenosis before PMBV than in healthy subjects [15.0 +/- 3.8 and 9.4 +/- 2.9 ng/ml; p < 0.001, respectively]. There were no significant differences between patients with mitral stenosis after PMBV and healthy subjects [10.9 +/- 3.1 and 9.4 +/- 2.9 ng/ml; p = 0.09, respectively]. There was a significant positive correlation between tenascin-C levels and sPAP [r = 0.508, p < 0.001]. In multivariant analysis, tenascin-C predicted mitral stenosis [p = 0.004, OR: 2.31]. Tenascin-C was an independent predictor for rheumatic mitral stenosis