scholarly journals The Relationship between Vitamin D Metabolites and Androgens in Women with Polycystic Ovary Syndrome

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1219
Author(s):  
Jakub Mesinovic ◽  
Helena J. Teede ◽  
Soulmaz Shorakae ◽  
Gavin W. Lambert ◽  
Elisabeth A. Lambert ◽  
...  

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among women of reproductive age, with hyperandrogenism present in up to 90% of affected women. Some evidence suggests a link between vitamin D deficiency and PCOS features via insulin resistance and inflammation. Our aim was to explore the relationship between biochemical markers of vitamin D status and androgens in women with PCOS. This cross-sectional study used bio-banked samples from 46 pre-menopausal women with PCOS (mean ± SD: age 30 ± 6 years; BMI 29 ± 6 kg/m2). We measured 25-hydroxyvitamin D (25[OH]D), vitamin D-binding protein (DBP), total testosterone, sex hormone-binding globulin (SHBG), and calculated the free androgen index (FAI) and bioavailable and free 25(OH)D. Fasting glucose and insulin were used to calculate the homeostatic model assessment of insulin resistance (HOMA-IR) and body fat percentage was determined via dual energy x-ray absorptiometry. High-sensitivity C-reactive protein (hs-CRP) was measured as a marker of inflammation. DBP was positively associated with total 25(OH)D and expectedly, negatively associated with free 25(OH)D. There were no associations between vitamin D metabolites and total testosterone, SHBG or FAI, even after adjusting for age, body fat percentage, HOMA-IR and hs-CRP. We found no associations between vitamin D metabolites and androgens in women with PCOS. Studies that have identified a vitamin D–androgen link have largely relied on methodology with numerous pitfalls; future studies should exclusively use gold-standard measures to confirm these findings in this population.

2021 ◽  
Vol 12 ◽  
pp. 204201882110496
Author(s):  
Gurhan Guney ◽  
Mine Islimye Taskin ◽  
Ozgur Baykan ◽  
Ertan Adali ◽  
Selin Gul Tezcan ◽  
...  

Background: Polycystic ovary syndrome is known to be the most common hormonal disorder in women of reproductive age. Current evidence shows that regulatory proteins secreted from the adipose tissue called adipokines may have a role in polycystic ovary syndrome. We planned to investigate the role of endotrophin that has never been researched in polycystic ovary syndrome before and its correlation with other metabolic parameters and adipokines such as adiponectin and ghrelin in patients with polycystic ovary syndrome. Methods: Forty-three women ( n: 43) with polycystic ovary syndrome and 43 ( n: 43) women as a control group were enrolled in this cross-sectional study. Serum levels of endotrophin, adiponectin, and ghrelin levels were measured with the enzyme-linked immunosorbent assay method. High-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol levels, luteinizing hormone/follicle-stimulating hormone ratio, total testosterone, and triglyceride levels were measured. Homeostasis model assessment for insulin resistance index, body mass index, Ferriman Gallwey Score, and waist-to-hip ratio were also evaluated. Results: Total testosterone, homeostasis model assessment for insulin resistance, C-reactive protein, luteinizing hormone/follicle-stimulating hormone ratio, and triglyceride levels were higher in patients with polycystic ovary syndrome ( p < 0.01). No difference was detected between the groups in terms of body mass index, Ferriman Gallwey Score, waist-to-hip ratio, total cholesterol, low-density lipoprotein, and high-density lipoprotein levels ( p > 0.05). We did not observe any significant difference in adiponectin and ghrelin levels between the groups ( p > 0.05). Patients with polycystic ovary syndrome had significantly higher endotrophin levels ( p < 0.01). According to our regression analyses [area under the curve: 0.973 (0.935–1.000), 95% confidence interval, 95.2% sensitivity, and 100% specificity], it was shown that endotrophin greater than 92 ng/ml and homeostasis model assessment for insulin resistance greater than 2.5 might be good predictors for polycystic ovary syndrome diagnosis. Conclusion: We demonstrated that endotrophin level is higher in patients with polycystic ovary syndrome and may have predicted polycystic ovary syndrome with increased homeostasis model assessment for insulin resistance index. There was no significant difference in adiponectin and ghrelin levels in the polycystic ovary syndrome group. Endotrophin may have a role in polycystic ovary syndrome etiology rather than other adipokines.


2015 ◽  
Vol 61 (3) ◽  
pp. 215-219 ◽  
Author(s):  
Margareth Chiharu Iwata ◽  
Livia Porquere ◽  
Isabel C. Espósito Sorpreso ◽  
Edmund C. Baracat ◽  
José Maria Soares Júnior

Summary Objective: Objective: to compare clinical and laboratory parameters in women with polycystic ovary syndrome (PCOS) using metformin or combined oral contraceptive (COC) after 6 months. Methods: retrospective study analyzing records of patients with PCOS using the Androgen Excess and Polycystic Ovary Syndrome (AE-PCOS) Society criteria. The groups were: I-COC (21 tablets, pause of 7 days; n=16); II-metformin (850mg 12/12h, n=16); III-COC plus metformin (n=9). Body mass index (BMI), acne (% of improvement), modified Ferriman-Gallway index and menstrual cycle index (MCI), luteinizing hormone (LH), follicle-stimulating hormone (FSH), total testosterone (TT), androstenedione (A) and homeostasis model assessment: insulin resistance (HOMA-IR) index were assessed Results: isolated use of COC compared to metformin was better regarding to acne, Ferriman index, MCI, LH, TT and A levels. On the other hand, metformin was better in the HOMA-IR index (4.44 and 1.67 respectively, p=0.0007). The association COC plus metformin, compared to metformin alone shows the maintenance of improvement of acne, Ferriman index, MCI, and testosterone levels. The HOMA-IR index remained lower in the metformin alone group (4.19 and 1.67, respectively; p=0,046). The comparison between COC plus metformin and COC alone, in turn, shows no difference in the improvement of acne, Ferriman index, MCI, LH, TT and A levels, indicating that the inclusion of metformin did not lead to additional benefits in these parameters. Still, the HOMA-IR index was similar in both groups (4.19 and 4.44 respectively; p=0.75), showing that the use of metformin associated with COC may not improve insulin resistance as much as it does if used alone. Conclusion: our data suggest that the combination of metformin and contraceptive does not improve insulin resistance as observed with metformin alone.


2015 ◽  
Vol 172 (2) ◽  
pp. 173-179 ◽  
Author(s):  
Magdalena Olszanecka-Glinianowicz ◽  
Paweł Madej ◽  
Michał Wdowczyk ◽  
Aleksander Owczarek ◽  
Jerzy Chudek

ObjectiveThe aim of this study was to analyse relationships between plasma fibroblast growth factor 21 (FGF21) levels and nutritional status, and metabolic and hormonal disturbances in polycystic ovary syndrome (PCOS) women.Design and settingA cross-sectional study involving 85 PCOS (48 obese) and 72 non-PCOS women (41 obese) was conducted to evaluate the relationship between FGF21 levels and PCOS.MethodsAnthropometric parameters and body composition were determined. In the fasting state; serum concentrations of glucose, androgens, FSH, LH, SHBG, insulin and FGF21 were measured.ResultsPlasma FGF21 levels were significantly higher in obese women compared with normal-weight women in both PCOS and non-PCOS subgroups (120.3 (18.2–698) vs 62.3 (16.4–323.6) pg/ml, P<0.05 and 87.2 (12.9–748.4) vs 62.9 (18.0–378.8) pg/ml, P<0.05 respectively). Additionally, circulating FGF21 levels were significantly higher in the obese PCOS subgroup compared with the non-PCOS subgroup (120.3 (18.2–698.0) vs 87.2 (12.9–748.4) pg/ml, P<0.05). Circulating FGF21 levels were proportional to BMI (R=0.27; P<0.001), body fat mass (R=0.24; P<0.01) and percentage (R=0.24; P<0.01), as well as waist circumference (R=0.26; P<0.01). Additionally, plasma insulin and homeostasis model assessment of insulin resistance (HOMA-IR) values were related to FGF21 levels (R=0.44; P<0.001 and R=0.19; P<0.05 respectively). In multiple regression analysis, circulating FGF21 level variability was explained by HOMA-IR values and fat percentage, as well as waist circumference, but not correlated with oestradiol levels and free androgen index values.ConclusionsHigher circulating FGF21 levels are related to nutritional status and insulin resistance independent of PCOS. Increased FGF21 is associated with metabolic but not hormonal disturbances.


2004 ◽  
Vol 89 (3) ◽  
pp. 1273-1276 ◽  
Author(s):  
Evanthia Diamanti-Kandarakis ◽  
Chryssa Kouli ◽  
Krystallenia Alexandraki ◽  
Giovanna Spina

Abstract Insulin resistance is a common metabolic feature of polycystic ovary syndrome (PCOS). In this study, we examined the validity of the mathematical indices [the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model of assessment (HOMA)] that calculate insulin sensitivity and their correlation to glucose utilization with the insulin infusion rate in 40 mU/m2·min by the euglycemic clamp (M) in women with PCOS. We studied 59 women with PCOS (20 lean, 16 overweight, and 23 obese subjects). Euglycemic clamp testing was performed, and QUICKI, HOMA, total testosterone, fasting insulin, fasting glucose, and glucose-to-insulin ratio were estimated. No difference was found in testosterone and glucose levels among the three groups. Lean or overweight women compared with obese women differed in insulin levels, glucose-to-insulin ratio, QUICKI, and HOMA (P &lt; 0.01). No statistical difference was found between lean and overweight women in the above parameters. M differed when lean women were compared with overweight (P &lt; 0.002) or obese women (P &lt; 0.0001); however, no statistical difference was observed between overweight and obese women. No significant correlation was found between M and QUICKI or HOMA. We conclude that mathematical indices should be applied with caution in different insulin-resistant populations and should not be considered a priori equivalent to the euglycemic clamp technique.


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