Effects of curcumin on body weight, glycemic control and serum lipids in women with polycystic ovary syndrome: A randomized, double-blind, placebo-controlled trial.

OBJECTIVE: The aim of this study was to evaluate the effect of curcumin on body weight, glycemic control and serum lipids in women suffering from polycystic ovary syndrome (PCOS). METHODS: The current randomized, double-blinded, placebo-controlled clinical trial was performed on 60 subjects with PCOS, aged 18-40 years old. Subjects were randomly allocated to take 500 mg/day curcumin (n = 30) or placebo (n = 30) for 12 weeks. Glycemic control and serum lipids were measured at baseline and after the 12-week intervention. Using RT-PCR method, gene expression related to insulin and lipid metabolism was evaluated. RESULTS: Curcumin significantly decreased weight (-0.8 ± 0.9 vs. -0.2 ± 0.8 kg, P = 0.03) and BMI (-0.3 ± 0.4 vs. -0.1 ± 0.3 kg/m2, P = 0.03). Curcumin, compared with the placebo, significantly reduced fasting glucose (ß -2.63 mg/dL; 95% CI, -4.21, -1.05; P = 0.002), serum insulin (ß -1.16 µIU/mL; 95% CI, -2.12, -0.19; P = 0.02), insulin resistance (ß -0.26; 95% CI, -0.48, -0.03; P = 0.02), and significantly increased insulin sensitivity (ß 0.006; 95% CI, 0.001, 0.01; P = 0.02). In addition, taking curcumin was associated with a significant reduction in total cholesterol (ß -15.86 mg/dL; 95% CI, -24.48, -7.24; P = 0.001), LDL-cholesterol (ß -16.09 mg/dL; 95% CI, -25.11, -7.06; P = 0.001) and total-/HDL-cholesterol ratio (ß -0.62; 95% CI, -0.93, -0.30; P < 0.001), and a significant increase in HDL-cholesterol levels (ß 2.14 mg/dL; 95% CI, 0.36, 3.92; P = 0.01) compared with the placebo. Additionally, curcumin administration up-regulated gene expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) (P = 0.03) and low-density lipoprotein receptor (LDLR) (P < 0.001) compared with the placebo. CONCLUSIONS: Overall, curcumin administration for 12 weeks to women with PCOS had beneficial effects on body weight, glycemic control, serum lipids except triglycerides and VLDL-cholesterol levels, and gene expression of PPAR-γ and LDLR. Registered under Clinical Trials.gov Identifier no. http://www.irct.ir: IRCT20170513033941N50.

The effects of resveratrol on metabolic status in patients with type 2 diabetes mellitus and coronary heart disease.

This study was performed to investigate the effects of resveratrol on metabolic status in patients with type 2 diabetes mellitus (T2DM) and coronary heart disease (CHD). This randomized, double-blind, placebo-controlled trial was performed with 56 patients having T2DM and CHD. The patients were randomly divided into two groups to receive either 500 mg resveratrol per day (n = 28) or placebo (n = 28) for 4 weeks. Resveratrol reduced fasting glucose (ß-10.04 mg dL-1; 95% CI, -18.23, -1.86; P = 0.01), insulin (ß-1.09 µIU mL-1; 95% CI, -1.93, -0.24; P = 0.01) and insulin resistance (ß-0.48; 95% CI, -0.76, -0.21; P = 0.001) and significantly increased insulin sensitivity (ß 0.006; 95% CI, 0.001, 0.01; P = 0.02) when compared with the placebo. Resveratrol also significantly increased HDL-cholesterol levels (ß 3.38 mg dL-1; 95% CI, 1.72, 5.05; P < 0.001) and significantly decreased the total-/HDL-cholesterol ratio (ß-0.36; 95% CI, -0.59, -0.13; P = 0.002) when compared with the placebo. Additionally, resveratrol caused a significant increase in total antioxidant capacity (TAC) (ß 58.88 mmol L-1; 95% CI, 17.33, 100.44; P = 0.006) and a significant reduction in malondialdehyde (MDA) levels (ß-0.21 µmol L-1; 95% CI, -0.41, -0.005; P = 0.04) when compared with the placebo. Resveratrol upregulated PPAR-γ (P = 0.01) and sirtuin 1 (SIRT1) (P = 0.01) in the peripheral blood mononuclear cells (PBMCs) of T2DM patients with CHD. Resveratrol supplementation did not have any effect on inflammatory markers. Four-week supplementation of resveratrol in patients with T2DM and CHD had beneficial effects on glycemic control, HDL-cholesterol levels, the total-/HDL-cholesterol ratio, TAC and MDA levels. Resveratrol also upregulated PPAR-γ and SIRT1 in the PBMCs of T2DM patients with CHD.