This systematic review and meta-analysis of randomized controlled trials (RCTs) was performed to summarize the effect of ginger intake on weight loss, glycemic control and lipid profiles among overweight and obese subjects. We searched the following databases through November 2017: MEDLINE, EMBASE, Web of Science, and Cochrane Central Register of Controlled Trials. The relevant data were extracted and assessed for quality of the studies according to the Cochrane risk of bias tool. Data were pooled using the inverse variance method and expressed as Standardized Mean Difference (SMD) with 95% Confidence Intervals (95% CI). Heterogeneity between studies was assessed by the Cochran Q statistic and I-squared tests (I). Overall, 14 studies were included in the meta-analyses. Fourteen RCTs with 473 subjects were included in our meta-analysis. The results indicated that the supplementation with ginger significantly decreased body weight (BW) (SMD -0.66; 95% CI, -1.31, -0.01; P = 0.04), waist-to-hip ratio (WHR) (SMD -0.49; 95% CI, -0.82, -0.17; P = 0.003), hip ratio (HR) (SMD -0.42; 95% CI, -0.77, -0.08; P = 0.01), fasting glucose (SMD -0.68; 95% CI, -1.23, -0.05; P = 0.03) and insulin resistance index (HOMA-IR) (SMD -1.67; 95% CI, -2.86, -0.48; P = 0.006), and significantly increased HDL-cholesterol levels (SMD 0.40; 95% CI, 0.10, 0.70; P = 0.009). We found no detrimental effect of ginger on body mass index (BMI) (SMD -0.65; 95% CI, -1.36, 0.06; P = 0.074), insulin (SMD -0.54; 95% CI, -1.43, 0.35; P = 0.23), triglycerides (SMD -0.27; 95% CI, -0.71, 0.18; P = 0.24), total- (SMD -0.20; 95% CI, -0.58, 0.18; P = 0.30) and LDL-cholesterol (SMD -0.13; 95% CI, -0.51, 0.24; P = 0.48). Overall, the current meta-analysis demonstrated that ginger intake reduced BW, WHR, HR, fasting glucose and HOMA-IR, and increased HDL-cholesterol, but did not affect insulin, BMI, triglycerides, total- and LDL-cholesterol levels.
Although several studies have evaluated the effect of folate supplementation on diabetes biomarkers among patients with metabolic diseases, findings are inconsistent. This review of randomized controlled trials (RCTs) was performed to summarize the evidence on the effects of folate supplementation on diabetes biomarkers among patients with metabolic diseases. Randomized-controlled trials (RCTs) published in PubMed, EMBASE, Web of Science and Cochrane Library databases up to 1 September 2017 were searched. Two review authors independently assessed study eligibility, extracted data, and evaluated risk of bias of included studies. Heterogeneity was measured with a Q-test and with I statistics. Data were pooled by using the fix or random-effect model based on the heterogeneity test results and expressed as standardized mean difference (SMD) with 95% confidence interval (CI). A total of sixteen randomized controlled trials involving 763 participants were included in the final analysis. The current meta-analysis showed folate supplementation among patients with metabolic diseases significantly decreased insulin (SMD -1.28; 95% CI, -1.99, -0.56) and homeostasis model assessment of insulin resistance (HOMA-IR) (SMD -1.28; 95% CI, -1.99, -0.56). However, folate supplementation did not affect fasting plasma glucose (FPG) (SMD -0.30; 95% CI, -0.63, 0.02) and hemoglobin A1C (HbA1c) (SMD -0.29; 95% CI, -0.61, 0.03). The results of this meta-analysis study demonstrated that folate supplementation may result in significant decreases in insulin levels and HOMA-IR score, but does not affect FPG and HbA1c levels among patients with metabolic diseases.
The current study was conducted to assess the effects of vitamin D supplementation on insulin metabolism, lipid fractions, biomarkers of inflammation, and oxidative stress in diabetic hemodialysis (HD) patients. This randomized double-blind placebo-controlled clinical trial was carried out among 60 diabetic HD patients. Subjects were randomly allocated into two groups to intake either oral vitamin D3 supplements at a dosage of 50 000 IU (n=30) or placebo (n=30) every 2 weeks for 12 weeks. After 12 weeks of intervention, subjects who received vitamin D supplements compared with the placebo had significantly decreased serum insulin concentrations (-3.4±3.7 vs. +2.0±4.2 μIU/ml, p<0.001), homeostasis model of assessment-estimated insulin resistance (HOMA-IR) (-1.2±1.8 vs. +0.9±2.3, p<0.001), and improved quantitative insulin sensitivity check index (QUICKI) (+0.02±0.03 vs. -0.01±0.02, p<0.001). In addition, compared with the placebo, vitamin D supplementation led to significant reductions in serum high-sensitivity C-reactive protein (hs-CRP) (-1.4±2.5 vs. +1.4±4.8 mg/l, p=0.007), plasma malondialdehyde (MDA) (-0.1±0.2 vs. +0.1±0.2 μmol/l, p=0.009) and a significant increase in plasma total antioxidant capacity (TAC) concentrations (+33.8±56.7 vs. -2.0±74.5 mmol/l, p=0.04). We did not see any significant effect of vitamin D supplementation on lipid profiles and other biomarkers of inflammation and oxidative stress compared with the placebo. Overall, we found that vitamin D supplementation had beneficial effects on serum insulin, HOMA-IR, QUICKI, serum hs-CRP, plasma MDA, and TAC levels among diabetic HD patients for 12 weeks. CLINICAL REGISTRATION:: http://www.irct.ir: IRCT201611155623N92.
Objective: This study was carried out to determine the effects of vitamin D supplementation on signaling pathway of inflammation and oxidative stress in diabetic hemodialysis (HD) patients.Methods: This randomized double-blind placebo-controlled clinical trial was conducted among 60 diabetic HD patients. Subjects were randomly allocated into two groups to intake either vitamin D supplements at a dosage of 50,000 IU (n = 30) or placebo (n = 30) every 2 weeks for 12 weeks. Gene expression of inflammatory cytokines and biomarkers of oxidative stress were assessed in peripheral blood mononuclear cells (PBMCs) of diabetic HD patients with RT-PCR method.Results: Results of RT-PCR indicated that after the 12-week intervention, compared to the placebo, vitamin D supplementation downregulated gene expression of interleukin (IL)-1β (P = 0.02), tumor necrosis factor alpha (TNF-α) (P = 0.02) and interferon gamma (IFN-γ) (P = 0.03) in PBMCs of diabetic HD patients. Additionally, vitamin D supplementation, compared to the placebo, downregulated gene expression of transforming growth factor beta (TGF-β) (P = 0.04), protein kinase C (PKC) (P = 0.001), and mitogen-activated protein kinases 1 (MAPK1) (P = 0.02) in PBMCs of diabetic HD patients. Although not significant, vitamin D supplementation let to a reduction of nuclear factor kappa B (NF-kB) (p = 0.75) expression in PBMCs isolated from diabetic patients compared to the placebo group. There was no statistically significant change following supplementation with vitamin D on gene expression of interleukin (IL)-4, IL-6, and vascular endothelial growth factor (VEGF) in PBMCs of diabetic HD patients.Conclusions: Overall, we found that vitamin D supplementation for 12 weeks among diabetic HD patients had beneficial effects on few gene expression related to inflammation and oxidative stress.Clinical trial registration: IRCT201701035623N101. Registered on January 8, 2017.
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