Metabolic Response to Selenium Supplementation in PCOS
Metabolic Response to Selenium Supplementation in PCOS
In the present study, 70 women met the inclusion criteria based on Rotterdam criteria and were enrolled in the study. The groups were well-matched for age and BMI. Among individuals in the selenium group, three women [withdraw due to personal reasons (N = 3)] and in the placebo group, two women [withdraw due to personal reasons (N = 2)] did not complete the trial. However, as the analysis was carried out based on ITT, all 70 PCOS women were included in the final analysis. On average, the rate of compliance in our study was high, such that higher than 90% of tablets were taken throughout the study in both groups. No side effects were reported following the consumption of selenium supplements in patients with PCOS throughout the study.
Mean baseline BMI of study participants was 25·2 ± 3·9 kg/m (range: 16·0–35·0 kg/m). Mean age and height of study participants were not statistically different between selenium and placebo groups. Baseline weight and BMI as well as their means before and after intervention were not significantly different comparing the two groups (Table 1).
Based on the 3-day dietary records obtained throughout the intervention, no statistically significant difference was seen between the two groups in terms of dietary intakes of energy, carbohydrates, proteins, fats, saturated fatty acids (SFA), polyunsaturated fatty acids (PUFA), monounsaturated fatty acids (MUFA), cholesterol, total dietary fibre (TDF) and selenium (Table 2).
After 8 weeks of intervention, subjects who received selenium supplements had significantly decreased serum insulin levels (−29·83 ± 47·29 vs +9·07 ± 77·12 pmol/l, P = 0·013), HOMA-IR (−1·15 ± 1·81 vs +0·42 ± 3·09, P = 0·011), HOMA-B (−19·06 ± 30·95 vs +4·55 ± 47·99, P = 0·017) and increased QUICKI (+0·03 ± 0·04 vs +0·0009 ± 0·05, P = 0·032) compared with placebo (Table 3). In addition, supplementation with selenium resulted in a significant reduction in serum triglycerides (−0·14 ± 0·55 vs +0·11 ± 0·30 mmol/l, P = 0·025) and VLDL-C concentrations (−0·03 ± 0·11 vs +0·02 ± 0·06 mmol/l, P = 0·025) compared with placebo. We did not see any significant effects of selenium supplementation on FPG, other lipid profiles and waist and hip circumference. Within-group changes showed a significant reduction in serum insulin levels (P = 0·001), HOMA-IR (P = 0·001), HOMA-B (P = 0·001) and a significant rise in QUICKI (P = 0·002) in the selenium group. In addition, within-group changes revealed a significant increase in serum triglycerides (P = 0·047), VLDL-C (P = 0·047) and a significant reduction in LDL-C concentrations (P = 0·023) in the placebo group.
Baseline levels of FPG were significantly different between the two groups. Therefore, we controlled the analyses for the baseline levels. However, after this adjustment no significant changes in our findings occurred, except for FPG (P = 0·009) (Table 4). Additional adjustments for age and baseline BMI did not affect our findings, except for FPG (P = 0·010).
Results
In the present study, 70 women met the inclusion criteria based on Rotterdam criteria and were enrolled in the study. The groups were well-matched for age and BMI. Among individuals in the selenium group, three women [withdraw due to personal reasons (N = 3)] and in the placebo group, two women [withdraw due to personal reasons (N = 2)] did not complete the trial. However, as the analysis was carried out based on ITT, all 70 PCOS women were included in the final analysis. On average, the rate of compliance in our study was high, such that higher than 90% of tablets were taken throughout the study in both groups. No side effects were reported following the consumption of selenium supplements in patients with PCOS throughout the study.
Mean baseline BMI of study participants was 25·2 ± 3·9 kg/m (range: 16·0–35·0 kg/m). Mean age and height of study participants were not statistically different between selenium and placebo groups. Baseline weight and BMI as well as their means before and after intervention were not significantly different comparing the two groups (Table 1).
Based on the 3-day dietary records obtained throughout the intervention, no statistically significant difference was seen between the two groups in terms of dietary intakes of energy, carbohydrates, proteins, fats, saturated fatty acids (SFA), polyunsaturated fatty acids (PUFA), monounsaturated fatty acids (MUFA), cholesterol, total dietary fibre (TDF) and selenium (Table 2).
After 8 weeks of intervention, subjects who received selenium supplements had significantly decreased serum insulin levels (−29·83 ± 47·29 vs +9·07 ± 77·12 pmol/l, P = 0·013), HOMA-IR (−1·15 ± 1·81 vs +0·42 ± 3·09, P = 0·011), HOMA-B (−19·06 ± 30·95 vs +4·55 ± 47·99, P = 0·017) and increased QUICKI (+0·03 ± 0·04 vs +0·0009 ± 0·05, P = 0·032) compared with placebo (Table 3). In addition, supplementation with selenium resulted in a significant reduction in serum triglycerides (−0·14 ± 0·55 vs +0·11 ± 0·30 mmol/l, P = 0·025) and VLDL-C concentrations (−0·03 ± 0·11 vs +0·02 ± 0·06 mmol/l, P = 0·025) compared with placebo. We did not see any significant effects of selenium supplementation on FPG, other lipid profiles and waist and hip circumference. Within-group changes showed a significant reduction in serum insulin levels (P = 0·001), HOMA-IR (P = 0·001), HOMA-B (P = 0·001) and a significant rise in QUICKI (P = 0·002) in the selenium group. In addition, within-group changes revealed a significant increase in serum triglycerides (P = 0·047), VLDL-C (P = 0·047) and a significant reduction in LDL-C concentrations (P = 0·023) in the placebo group.
Baseline levels of FPG were significantly different between the two groups. Therefore, we controlled the analyses for the baseline levels. However, after this adjustment no significant changes in our findings occurred, except for FPG (P = 0·009) (Table 4). Additional adjustments for age and baseline BMI did not affect our findings, except for FPG (P = 0·010).
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