Polycystic Ovary Syndrome
Conditions
Keywords
PCOS, vitamin D, insulin resistance, glycemic control
Brief summary
The study tests the hypothesis that correction of vitamin D deficiency among women with PCOS will improve insulin sensitivity and resistance and inflammatory response to PCOS.
Detailed description
Polycystic ovary syndrome (PCOS) is a common complex and heterogenous endocrine disorder. It affects ≤10% of women of reproductive age, with approximately 16%-80% of the affected women being obese. Polycystic ovary syndrome frequently is associated with insulin resistance (IR) accompanied by compensatory hyperinsulinemia, and IR is aggravated by the interaction between obesity and the syndrome. Moreover, the contribution of body mass and/or body fat distribution to IR of PCOS remains controversial. In addition, women with PCOS with IR are at an increased risk of developing diabetes, hypertension, dyslipidemia and atherosclerosis. Preliminary data on the local women with PCOS showed high prevalence of vitamin D deficiency (serum 25(OH)D \< 50 nmol/L). Recent studies showed that vitamin D deficiency is linked to IR, type 2 diabetes mellitus, obesity, inflammation and cardio vascular disease. Several studies have demonstrated that serum 25(OH)D levels were negatively correlated with body mass index (BMI), body fat, and IR. These conditions are common among women with PCOS. Accordingly, it is anticipated that vitamin D deficiency and/or insufficiency may contribute to the endocrine and metabolic disarrangements among women with PCOS. Such adverse effects may further contribute to the risk of further long term complications among women with PCOS.
Interventions
DIETARY_SUPPLEMENTVitamin D3 pills
Dietary supplement
OTHERPlacebo pills
Placebo pills similar in appearance and shape but without vitamin D
Sponsors
King Abdulaziz University
Study design
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
FEMALE
Age
20 Years to 45 Years
Healthy volunteers
No
Inclusion criteria
PCOS diagnosis to include three of the Rotterdam criteria
Exclusion criteria
pregnancy lactation taking vitamin d or calcium supplement in excess of a regular multivitamins diabetes mellitus uncontrolled hypertension liver disease renal disease secondary causes of hyperandrogenism metabolic bone disease thyroid dysfunction taking oral contraceptives taking hypoglycemic agents (metformin or thiazolidinediones) medication to affect plasma sex steroids for \>/3 months before the study smokers
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Correction of vitamin D deficiency improves insulin resistance compared to placebo | 24 weeks | The primary endpoint was an improvement in insulin resistance parameters \[Fasting serum insulin,glucose-to-insulin ratio (GIR) and homeostasis model assessment (HOMA) \] from baseline and at 24 weeks in vitamin D supplemented as compared with placebo groups. |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Insulin sensitivity | 24 weeks | Secondary endpoints were changes in parameter of insulin sensitivity\[ quantitative insulin sensitivity check index (QUICKI)\], among vitamin D supplemented group vs placebo group from baseline and at the end of the trial |
Other
| Measure | Time frame | Description |
|---|---|---|
| Exploratory outcomes: lipid profile | 24 weeks | Other endpoints were changes in lipid profile (total cholesterol, HDL-c, LDL-c, and triglycerides) |
| Exploratory outcomes: liver and renal function tests | 24 weeks | Other endpoints were changes in liver function tests \[albumin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase(ALP)\]; renal function tests (cystatine C, uric acid, urea) and parathyroid hormone (PTH) |
| Exploratory outcomes: vitamin D status | 24 weeks | Other endpoints were changes in serum 25-hydroxyvitamin D |
| Exploratory outcomes: endocrine profile | 24 weeks | Other endpoints were changes in (follicle-stimulating hormone, luteinizing hormone, prolactin, thyroid-stimulating hormone, free thyroxine, total testosterone, dehydroepiandrosterone (DHEA), DHEA sulfate, delta 4-androstenedione and sex-hormone binding globulin). |
| Exploratory outcomes: glycemic control | 24 weeks | Other endpoints were changes in HbA1c, fasting plasma glucose and fasting plasma insulin |
| Exploratory and safety outcome | 24 weeks | Other endpoints were changes in inflammatory markers (hs-CRP) |
Countries
Saudi Arabia
Contacts
Primary ContactMohammed-Salleh M Ardawi, PhD, FRCPath
Backup ContactAbdulrahim A Rouzi, FRCPC
Outcome results
None listed