Serum concentrations of betatrophin and its association with indirect indices of insulin resistance and beta cell function in women with polycystic ovary syndrome

Author(s):  
Agnieszka Adamska ◽  
Agnieszka Lebkowska ◽  
Malgorzata Jacewicz ◽  
Anna Krentowska ◽  
Justyna Hryniewicka ◽  
...  
Author(s):  
Dimitrios Panidis ◽  
Djuro Macut ◽  
Dimitrios Farmakiotis ◽  
David Rousso ◽  
Anargyros Kourtis ◽  
...  

1996 ◽  
pp. 126-141
Author(s):  
David A. Ehrmann ◽  
Jeppe Sturis ◽  
Maria M. Byrne ◽  
Robert L. Rosenfield ◽  
Kenneth S. Polonsky

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Agnieszka Adamska ◽  
Agnieszka Łebkowska ◽  
Małgorzata Jacewicz ◽  
Anna Krentowska ◽  
Justyna Hryniewicka ◽  
...  

Introduction. Data underline the role of betatrophin in glucose homeostasis. Polycystic ovary syndrome (PCOS) is characterized by insulin resistance (IR). The aim of our study was to investigate the relationship of serum betatrophin concentrations with indirect indices of IR and insulin secretion in women with PCOS, compared to the control group. Methods. The study group comprised 43 women with PCOS and 16 controls. IR was assessed by HOMA-IR and Matsuda index. Insulin secretion was evaluated with HOMA-B. An oral glucose tolerance test (OGTT) with estimation of serum betatrophin concentrations was performed. Results. Glucose load resulted in an increase in serum betatrophin concentrations in the control group (p=0.02). Serum betatrophin concentrations at 120 min of OGTT were lower in women with PCOS than in the control group (p=0.02). We observed positive correlations between baseline serum betatrophin concentrations and HOMA-IR (r=0.39, p=0.008), negative correlations with Matsuda index (r=−0.31, p=0.004), and a positive relationship with HOMA-B (r=0.38, p=0.01) in women with PCOS. Multiple regression analysis revealed that HOMA-B (β=0.47, p=0.001) was an independent factor connected to serum betatrophin levels in PCOS. Conclusions. Serum concentrations of betatrophin are connected with insulin resistance and beta cell function and did not change after glucose load in women with PCOS.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Bingjie Zhang ◽  
Jing Wang ◽  
Shanmei Shen ◽  
Jiayi Liu ◽  
Jie Sun ◽  
...  

Women with polycystic ovary syndrome (PCOS) show high prevalence of glucose intolerance. This study aimed to investigate the association of androgen excess with glucose intolerance in PCOS. A total of 378 women with PCOS participated in the study. Free androgen index (FAI) was selected as indicator of hyperandrogenism. Insulin sensitivity was assessed by 1/homeostasis model assessment of insulin resistance (1/HOMA-IR) and Matsuda insulin sensitivity index (ISIM); β-cell function was assessed by disposition index (DI). We found that women with glucose intolerance had higher FAI levels compared to women with normal glucose tolerance (NGT) (prediabetes 6.2, T2DM 7.9 versus NGT 5.0, resp.; p<0.001). Furthermore, there was a direct association between FAI levels and frequency of glucose intolerance (OR = 2.480, 95% CI 1.387–4.434), even after adjusting for age, BMI, waist circumference, hypertension, fasting insulin, testosterone, SHBG, and family history of diabetes. In addition, with FAI increase, glycosylated hemoglobin (HbA1c), plasma glucose concentrations, and serum insulin levels increased, while insulin sensitivity and β-cell function decreased. Our results suggested that androgen excess indicated by high FAI levels might serve as indicator of glucose intolerance, as it might promote insulin resistance and β-cell dysfunction in women with PCOS.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A319-A320
Author(s):  
Vishwanath Pattan ◽  
Maria Chang Villacreses ◽  
Rudruidee Karnchanasorn ◽  
Wei Feng ◽  
Raynald Samoa ◽  
...  

Abstract Trace element is essential for the proper growth, development, and physiology of the organism and the primary source of trace element is dietary intake. Among trace elements, the role of copper (Cu), selenium (Se), and zinc (Zn) in the pathogenesis of diabetes have been widely recognized. However, there is little information available about these 3 trace elements across the different states of glucose tolerance. We examined associations between serum levels of trace elements - Cu, Zn, and Se with various stages of glucose tolerance in a representative, cross-sectional sample of US adults. Our sample included 5,087 adults (≥20 years) with available serum concentrations of Cu, Zn and Se as well as states of glucose tolerance, defined by history, HbA1c, fasting, and 2-hour plasma glucose concentrations. Serum concentrations of trace elements were compared with glucose tolerance status with the consideration of covariates. Regression analyses was used to examine the relationship of trace elements with HOMA-IR, HOMA-B, and BMI in non-diabetic subjects with the consideration of appropriate covariates. Serum Se (P&lt;0.0001) and Zn (P&lt;0.0001) concentrations differed significantly among 3 groups based on the states of glucose tolerance, while no difference was noted in serum Cu concentration. In non-diabetic subjects, serum Cu concentration was positively correlated with BMI (P&lt;0.0001) with a possible compensatory increased beta cell function (P=0.018). Serum Se concentration was negatively correlated with insulin resistance (P=0.016) but not with beta cell function or BMI. Serum Zn concertation was negatively correlated with beta cell function (P=0.0023) and BMI (P=0.018), but not with insulin resistance. We found that a higher serum concentration of trace elements was associated with negative glucose and fuel homeostasis in a non-deficiency population possibly through different mechanisms. Although the casual relationship remains to be elucidated, we recommend against trace element supplementation in a non-deficiency population.


2019 ◽  
Vol 9 (1-s) ◽  
pp. 433-436 ◽  
Author(s):  
Mudasir Maqbool ◽  
Mohmad Amin Dar ◽  
Imran Gani ◽  
Mohammad Ishaq Geer

Polycystic Ovary Syndrome (PCOS) is the most common, yet complex, endocrine disorder affecting women in their reproductive years and is a leading cause of infertility. This disease appears to be multifactorial and polygenic in nature involving multisystem dysfunction, namely reproduction, endocrine and metabolic. Hyperandrogenism and insulin resistance appear to be central cause to the pathophysiology of the disease. The glucose and insulin metabolism pathways have been studied and debated to understand whether Insulin Resistance is due to a defect in insulin action or a primary defect in β-cell function or decreased hepatic clearance of insulin, or a combination of all these factors. Numerous studies have demonstrated that obese, normal weight and thin women with PCOS have a form of insulin resistance that is unique and intrinsic to the disorder. Moreover obese women with PCOS possess an additional burden of insulin resistance resulting from their excess adiposity. Hyperinsulinemia leads to increase in androgen production directly by acting as a co-gonadotropin, augmenting Luteinizing Hormone activity within the ovary, and indirectly by increasing serum LH pulse amplitude. Whereas Androgens may in turn contribute at least partially to the insulin resistance state linked with PCOS.  In this review, we will briefly study the role of insulin resistance in polycystic ovary syndrome. Keywords: Polycystic ovary syndrome, insulin resistance, Hyperandrogenism.


2020 ◽  
Vol 9 (3) ◽  
pp. 732 ◽  
Author(s):  
Aleksandra Maria Polak ◽  
Agnieszka Adamska ◽  
Anna Krentowska ◽  
Agnieszka Łebkowska ◽  
Justyna Hryniewicka ◽  
...  

Insulin resistance and hyperandrogenemia observed in polycystic ovary syndrome (PCOS) are associated with metabolic disturbances and could be connected with body composition pattern. To date, several studies defining the parameters of body composition using dual energy X-ray absorptiometry (DXA) method in the group of PCOS patients have been published, however, without the analysis in different phenotypes. The aim of the present study was to investigate the relationships between serum androgens concentration, insulin resistance and distribution of fat mass using DXA method in various PCOS phenotypes according to the Rotterdam criteria. We examined 146 women: 34 (38%) had PCOS phenotype A, 20 (23%) phenotype B, 20 (23%) phenotype C and 15 (16%) phenotype D (with mean age of each phenotype 25 years), and 57 control subjects (mean age of 25.5 years). Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Serum concentrations of testosterone, androstenedione and dehydroepiandrosterone sulfate (DHEA-S) were assessed and free androgen index (FAI) was calculated. In phenotypes A, B and C, we observed higher FAI in comparison to the control group (all p < 0.01). Serum concentrations of androstenedione and DHEA-S were higher in phenotypes A and C in comparison to the control group (all p < 0.01). However, only in phenotype A we found higher visceral adipose tissue (VAT) mass and android/gynoid ratio (A/G ratio) in comparison to the control group (all p < 0.01). In phenotype A, we observed connection of VAT with FAI (r = 0.58, p < 0.01). Accordingly, A/G ratio was related with FAI in all phenotypes (all p < 0.05). Additionally, in phenotype C, A/G ratio was related to serum concentrations of DHEA-S and androstenedione (r = 0.46, p = 0.03; r = 0.53, p = 0.01, respectively). We also found connections of HOMA-IR with VAT and A/G ratio in all phenotypes (all p < 0.05). Women with phenotype A had higher amount of VAT and A/G ratio in comparison to the control group. Serum concentration of androgens and insulin resistance are connected with VAT and A/G ratio in normoandrogenic and hyperandrogenic PCOS phenotypes.


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