The aim of this study was to investigate the effects of vitamin D supplementation on serum aminotransferases, insulin resistance, oxidative stress, and inflammatory biomarkers in adult patients with non-alcoholic fatty liver disease (NAFLD). Fifty-three patients with NAFLD were enrolled in a parallel, double-blind, placebo-controlled study. The patients were randomly allocated to receive either one oral pearl consisting of 50,000 IU vitamin D3 (n = 27) or a placebo (n = 26), every 14 days for 4 months. Serum aminotransferases, high-sensitive C-reactive protein (hs-CRP), tumor necrosis factor α, malondialdehyde (MDA), total antioxidant capacity, transforming growth factor β1, as well as grade of hepatic steatosis and homeostasis model assessment of insulin resistance were assessed pre- and post-intervention. In patients who received vitamin D supplement compared to the controls, the median of serum 25(OH)D3 significantly increased (16.2 vs. 1.6 ng/ml, P < 0.001). This increase accompanied by significant decrease in serum MDA (-2.09 vs. -1.23 ng/ml, P = 0.03) and near significant changes in serum hs-CRP (-0.25 vs. 0.22 mg/l, P = 0.06). These between-group differences remained significant even after controlling for baseline covariates. Other variables showed no significant changes. Improved vitamin D status led to amelioration in serum hs-CRP and MDA in patients with NAFLD. This might be considered as an adjunctive therapy to attenuate systemic inflammation and lipid peroxidation alongside other treatments for NAFLD patients.
Background: Non-alcoholic fatty liver disease (NAFLD) is a major worldwide public health problem with no effective treatment options. Green coffee bean extract (GCBE) is a rich source of bioactive phytochemicals with a variety of biochemical and physiological effects. Objectives: The aim of this study was to investigate the effects of GCBE on the management of patients with NAFLD. Methods: 44 patients with NAFLD were enrolled in a parallel, double-blind, placebo-controlled clinical trial. The participants were administered either GCBE or placebo (1 gram/day) for 8 weeks. They also were advised to follow a standard energy-balanced diet and physical activity. Liver ultrasonography, anthropometric variables, and biochemical parameters were compared at pre-and post-intervention.
Evidence has revealed that vitamin D status is associated with the cardiometabolic risk factors. Moreover, few gender-specific analyses have been performed in the clinical trials regarding vitamin D supplementation. As a result, assessing gender differences regarding the effects of vitamin D supplementation on some cardiometabolic biomarkers in patients with non-alcoholic fatty liver disease (NAFLD) was the aim of present study. We conducted a post hoc subgroup analysis of a double blind placebo controlled study. Patients with NAFLD randomly allocated to receive one oral pearl consisting of 50,000 IU vitamin D3 (n = 27, 13 men and 14 women) or a placebo (n = 26, 13 men and 13 women) every 14 days for four months. Serum lipid profiles, aminotransferases, high-sensitive C-reactive protein (hs-CRP), adiponectin as well as insulin resistance and dietary intakes were assessed pre- and post-study. In both genders, serum 25(OH) D3 increased significantly (P < 0.001). This increase was accompanied by significant decrease in serum total cholesterol (TC) (% of change: -7% in vitamin D vs. + 0.4% in placebo, P = 0.04) and LDL-C (%of change: -9.6% in vitamin D vs. -4% in placebo, P = 0.006) in women. However, in men, vitamin D supplementation increased the levels of serum TC (% of change: +9.2% in vitamin D vs. -10% in placebo, P = 0.02) with no significant effects on LDL-C. Moreover, vitamin D significantly reduced serum hs-CRP in women. The median daily calcium intake in both genders was well below the dietary reference intake for adults. In conclusion, improved vitamin D status might decrease serum TC and LDL-C levels as well as hs-CRP in women with NAFLD. However, it might increase serum TC in men who have low daily calcium intake. Further studies with larger sample sizes are needed to confirm these results.
Intrafamilial transmission of HCV is not the significant transmission route and sexual transmission does not seem to play a role in the intrafamilial spread of HCV infection. Intrafamilial transmission of HCV is possible but occurs at a low rate.
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