Akram Vatannejad, Amir Ali Sohrabpour, Soraiya Ebrahimpour-Koujan, Ahmad Esmaillzadeh, Edward Giovannucci
Journal: Nutrition journal 2024;23(1):24
PMID: 38413933
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a liver condition caused by excess fat accumulation and is linked to obesity, poor blood sugar control, and inflammation. Over time, MASLD can lead to liver fibrosis (a process where scar tissue builds up, affecting liver function). Vitamin D helps support the immune system and may protect the liver by acting through specific receptors and genetic pathways that control cell function and scarring. This study aimed to explore whether vitamin D supplementation could reduce liver fibrosis-related factors in patients with MASLD. This research was an exploratory randomised clinical trial. Patients with MASLD were randomly assigned to receive vitamin D supplementation (2000 IU/day) or no supplementation for 12 weeks. The results showed that compared to placebo, vitamin D supplementation increased vitamin D receptor (VDR) expression in liver tissue, decreased markers associated with liver scarring, changed certain gene signals linked to liver scarring, suggesting vitamin D can affect how liver cells work, and did not cause serious side effects. High density lipoprotein cholesterol was also improved. The authors concluded that vitamin D may help reduce liver fibrosis risk in MASLD by modulating genetic and molecular pathways linked to scarring. These findings are clinically relevant for healthcare practitioners because they highlight the potential for vitamin D as a low-risk, accessible intervention to help prevent or slow the progression of liver fibrosis in MASLD patients.
BACKGROUND AND AIMS
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a global metabolic problem which can lead to irreversible liver fibrosis. It has been shown that vitamin D and its receptors contribute to fibrogenic pathways in the liver. However, the effect of vitamin D supplementation on liver fibrosis related factors have not been examined. This double blinded placebo controlled clinical trial was designed to investigate the effects on vitamin D supplementation on serum levels of VDR, fibrogenic factors and fibrogenic MicroRNAs in MASLD patients.
METHODS
Forty six MASLD patients after block matching for sex and BMI were randomly assigned to receive 4000 IU/d vitamin D or placebo for 12 weeks. Weight, height and waist circumference were measured. Serum fibrogenic microRNAs, laminin, collagen type IV, hyaluronic acid, vitamin D, VDR, PTH, blood fasting glucose, serum fasting insulin, lipid profile, ALT and AST were determined at the baseline and at the end of the trial. Insulin resistance and insulin sensitivity were calculated using the HOMA-IR and QUICKI equation.
RESULTS
Supplementation with vitamin D for 12 weeks led to the significant increases in serum 25(OH) vitamin D, VDR and HDL-C compared to placebo (P < 0.001, P = 0.008 and P < 0.001). There were significant decreases in ALT, AST, FBS and LDL-C levels in the vitamin D group as compared to the placebo (P < 0.05). Laminin and hyaluronic acid concentrations were significantly decreased in the vitamin D group as compared to the placebo group, by -10.6 and - 28.7 ng/mL, respectively. Supplementation with vitamin D for 12 weeks resulted in a significant lower MiR-21 and MiR-122 gene expressions compared to the placebo group (P = 0.01 and P < 0.001, respectively).
DISCUSSION
As the first randomized controlled trial on the effect of vitamin D supplementation on serum levels of VDR, fibrogenic factors and fibrogenic MicroRNAs in MASLD patients, we found a significant reduction in some liver fibrogenic factors, in liver transaminases and corresponding changes in some fibrosis-related MiRs and some metabolic factors. Further clinical trials with larger sample sizes and direct measures of liver fibrosis are needed to confirm these findings.
TRIAL REGISTRATION NUMBER
(available at: http://www.irct.ir , identifier: IRCT201405251485N13), Registration date: 14-03-2017.
© 2024. The Author(s).
© Copyright 2026, Nutrition Evidence
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