Abstract
Background: Data on the effects of omega-3 fatty acid supplementation on clinical symptoms and metabolic profiles in patients with endometrial hyperplasia (EH) are limited. This intervention was performed to assess the effects of omega-3 fatty acid supplementation on clinical symptoms and metabolic profiles in patients with endometrial hyperplasia (EH). Methods: This randomized, double-blind, placebo-controlled trial was conducted among 40 women diagnosed with simple endometrial hyperplasia (EH). EH diagnosis was performed based on specific diagnostic procedures of biopsy. Participants were randomised into two groups to intake 1,000 mg omega-3 fatty acid supplements from flaxseed oil (n = 20) or placebo (n = 20), twice a day for 12 weeks. Fasting blood samples were taken at baseline and after the 12-week intervention to determine related markers. Results: Compared with the placebo, omega-3 fatty acid supplementation significantly decreased fasting plasma glucose (FPG) (-7.1 ± 9.6 vs. +2.0 ± 4.9 mg/dL, P = 0.001), serum insulin levels (-1.5 ± 4.6 vs. +1.6 ± 3.9 μIU/mL, P = 0.02) and homeostasis model of assessment-insulin resistance (HOMA-IR) (-0.4 ± 1.1 vs. +0.4 ± 1.0, P = 0.02). In addition, a significant increase in plasma total antioxidant capacity (TAC) (+102.6 ± 69.6 vs. +5.0 ± 37.1 mmol/L, P < 0.001) and total glutathione (GSH) levels (+63.6 ± 84.9 vs. -3.0 ± 69.4 μmol/L, P = 0.01) were seen following the supplementation of omega-3 fatty acid compared with the placebo. Omega-3 fatty acid supplementation had no significant effect on regression, lipid profiles, and other biomarkers of inflammation and oxidative. Conclusions: In conclusion, we found that omega-3 fatty acid administration for 12 weeks to subjects with EH significantly improved FPG, insulin, HOMA-IR, TAC and GSH levels, but did not influence regression, lipid profiles, and other biomarkers of inflammatory and oxidative stress.
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Key Points
Endometrial hyperplasia (EH) represents a spectrum of irregular morphological changes, whereby unusual proliferation of the endometrial glands leads an elevation in gland-to-stroma ratio when compared to endometrium from the proliferative phase of the cycle. It has reported that EH may led to endometrial cancer (EC) up to 50% of cases. The progress of inflammatory changes in EH may be considered as an important factor in the promotion of pathology, as well as an attributed risk factor for malignancy in EH.
High circulating and tissue contents of omega-3 fatty acid may be an important function in the prevention and treatment of cancer pathogenesis. Several studies have reported the beneficial effects of omega-3 fatty acid supplementation on markers of insulin metabolism, inflammation and oxidative stress in patients without EH. Based on existing evidence, the authors hypothesized that clinical signs, metabolic profiles, biomarkers of inflammation and oxidative stress of EH patients might be improved by omega-3 fatty acid supplementation. Data on the effects of omega-3 fatty acid supplementation on regression, glucose control, lipid concentrations, biomarkers of inflammation and oxidative stress in patients with EH are scarce. The purpose of the present study was to determine the effects of omega-3 fatty acid supplementation on regression and metabolic status of patients with EH. 40 EH patients were randomly assigned them to each take either 1mg of omega-3 flaxseed oil supplements or a placebo twice a day for 12 weeks. Supplementation with omega-3 significantly improved certain symptoms related to endometrial hyperplasia (EH), but not its inflammatory and oxidative stress biomarkers. After 12 weeks, the researchers reported that omega-3 fatty acid supplementation had significantly reduced the fasting plasma glucose by 7.1 mg/dl to 9.6mg/dl in the intervention group, compared to an increase of 2mg/dl to 4.9mg/dl in the placebo group.
Serum insulin levels in the intervention group had also seen a decrease of 1.5μIU/ml to 4.6μIU/ml, compared with an increase of 1.6μIU/ml to 3.9μIU/ml in the placebo group. Furthermore, there was a significant increase of 69.6mmol/L to 102.6mmol/L in the intervention group’s plasma total antioxidant capacity, versus a 5mmol/L to 37.1mmol/L increase in the placebo group. The intervention group’s total glutathione levels had also risen by 63.6 to 84.94μmol/L, compared to a decrease of 3μmol/L to 69μmol/L in the placebo group. However, the researchers also found that omega-3 fatty acid supplementation did not have any significant effect on regression, lipid profiles, or other biomarkers of inflammation and oxidative stress in EH. They noted that the study’s findings were consistent with those of previous studies, but also inconsistent with some past research that had found omega-3 fatty acid supplementation to be useful in reducing inflammation and oxidative stress. This discrepancy between this study and others might be mediated by distinct trial designs, various dosages of omega-3 fatty acid supplements, the source of omega-3 fatty acids, duration of the study, and variation in the individual characteristics of the subjects. However, the exact mechanism by which omega-3 fatty acids might influence fasting plasma glucose and markers of insulin metabolism is unknown. Improved markers of insulin metabolism by omega-3 fatty acid intake may be mediated by the inhibiting production of pro-inflammatory cytokines and gene expression levels of nuclear factor-κB (NF-κB). In conclusion, the study showed that omega-3 fatty acid administration for 12 weeks to subjects with EH significantly improved fasting plasma glucose, insulin, total antioxidant capacity and total glutathione levels, but did not influence regression and lipid profiles, and other biomarkers of inflammatory and oxidative stress. This suggests that omega-3 fatty acid supplementation may confer advantageous therapeutic potential for patients with EH. Further studies are needed in other participants and with longer periods to explore the plausible mechanism and confirm our findings.