Yan Meng

Objective: The purpose of the systematic review and meta-analysis was to determine if low-ratio n-6/n-3 long-chain polyunsaturated fatty acid (PUFA) supplementation affects serum inflammation markers based on the current studies. Methods: PubMed, Embase and The Cochrane library databases were systematically searched to find randomized controlled trials (RCTs) on the effect of low-ratio n-6/n-3 PUFA intervention on inflammation markers up to July 2020. Data were pooled using standardized mean difference (SMD) and 95% confidence intervals (95% CI), with P value ≦ 0.05 as statistical significance. Results: Thirty-one RCTs were included in the meta-analysis. The analysis indicated that increasing low-ratio n-6/n-3 PUFA supplementation decreased the level of tumor necrosis factor-α (TNF-α) (SMD = −0.270; 95% CI: −0.433, −0.106; P = 0.001) and interleukin 6 (IL-6) (SMD = −0.153; 95% CI: −0.260, −0.045; P = 0.005). There were no significant effects on C-reactive protein (CRP) (SMD = −0.027; 95% CI: −0.189: 0.135; P = 0.741). Subgroup analysis indicated that there was a significant reduction in TNF-α serum concentration in subjects from Asia (SMD: −0.367; 95% CI: −0.579, −0.155; P = 0.001) and in subjects with diseases (SMD: −0.281; 95% CI: −0.436, −0.127; P < 0.001). In the subgroup of the n-6/n-3 ratio ≦5, low-ratio n-6/n-3 PUFA supplementation could decrease the level of TNF-α (SMD: −0.335; 95% CI: −0.552, −0.119; P = 0.002). Serum IL-6 decreased significantly in patients from the Europe subgroup (SMD: −0.451; 95% CI: −0.688, −0.214; P < 0.001), but not in Asia (SMD: −0.034; 95% CI: −0.226, 0.157; P = 0.724), North America (SMD: −0.115; 95% CI: −0.274, 0.044; P = 0.157) and Oceania (SMD: 0.142; 95% CI: −0.557, 0.842; P = 0.690). Conclusion: Low-ratio n-6/n-3 PUFA supplementation could decrease significantly the concentration of serum TNF-α and IL-6, but not decrease CRP concentration.

Context: Vitamin D (VD) has been found to play a key role in nonalcoholic fatty liver disease (NAFLD). This meta-analysis explored the effects of VD supplementation in patients with NAFLD. Methods: The PubMed, EMBASE, and the Cochrane Library databases were searched to find randomized control trials (RCTs) that measured the changes between the VD supplement group and the control group until May 2019. Standard mean difference (SMD) with 95% confidence intervals (CI) was calculated when data units were different, otherwise weighted mean difference (WMD) and 95% CI was calculated. Heterogeneity was assessed using the I2 statistic. Results: Eight RCTs with 624 individuals were extracted. The main indicators, including serum alanine aminotransferase (WMD = -0.052; 95% CI: -3.740, 3.636; P = 0.978) and aspartate aminotransferase concentrations (WMD = -0.479; 95% CI: -2.791, 1.833; P = 0.685) were not significantly different between the intervention and placebo groups. In addition, no significant intergroup difference was observed in the following secondary indicators: fasting blood glucose (WMD = 0.466; 95% CI: -5.313, -10.879; P = 0.061), homeostasis model assessment (WMD = 0.380, 95% CI: -0.162, 0.923; P = 0.169), serum insulin concentration (WMD = 0.760; 95% CI: -0.532, 2.052; P = 0.249), high-density lipoprotein (WMD = -0.012; 95% CI: -0.188, 0.164; P = 0.891), and low-density lipoprotein (WMD = -0.115; 95% CI: -3.849, -3.620; P = 0.952). Conclusions: The results indicate that VD supplementation does not improve liver enzymes, insulin resistance, glucose metabolism parameters, and lipid levels in patients with NAFLD.