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Throughout the study, we assessed key health markers before and after supplementation, including liver function tests, lipid profiles, and glycaemic indices such as fasting blood glucose and insulin resistance. By the end of the trial, our findings indicated that vitamin D supplementation significantly improved fasting blood glucose levels and insulin resistance in the participants.
Specifically, we observed noteworthy increases in serum 25-hydroxy-vitamin D levels and reductions in fasting blood glucose and insulin resistance indicators. These results suggest that vitamin D might be an important player in improving metabolic health for those suffering from liver cirrhosis.
Our findings revealed that vitamin D not only helped reduce body weight and improve liver health, but it also played a role in restoring normal metabolic functions. By reducing inflammation and protecting liver cells from damage, vitamin D enhanced insulin sensitivity and affected fat metabolism positively.
Notably, we found that vitamin D helped inhibit a harmful process known as ferroptosis—a type of cell death linked to liver injury. Through various assays, we confirmed that vitamin D treatment boosted the liver's antioxidant capabilities and lessened iron buildup in liver cells. Overall, our research suggests that vitamin D could be a promising therapeutic option for individuals suffering from MAFLD.
Our research found that more than a third of these novel compounds displayed strong affinity for VDR and showed the ability to activate it. Among these, one compound, E15, stood out as particularly effective. It significantly inhibited the activation of hepatic stellate cells (HSCs), which play a critical role in the progression of liver fibrosis, thereby reducing the production of harmful extracellular matrix components.
Encouraged by these promising in vitro results, we proceeded to test E15 in a mouse model of liver fibrosis induced by carbon tetrachloride. The results were remarkable; E15 not only decreased fibrosis and collagen deposition, but also improved liver function without the negative side effect of hypercalcemia, which is often associated with traditional VDR agonists.
These findings suggest that E15 could be a powerful and safer alternative for addressing liver fibrosis, highlighting the significant therapeutic potential of targeting the vitamin D receptor in liver diseases.
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Our research found that more than a third of these novel compounds displayed strong affinity for VDR and showed the ability to activate it. Among these, one compound, E15, stood out as particularly effective. It significantly inhibited the activation of hepatic stellate cells (HSCs), which play a critical role in the progression of liver fibrosis, thereby reducing the production of harmful extracellular matrix components.
Encouraged by these promising in vitro results, we proceeded to test E15 in a mouse model of liver fibrosis induced by carbon tetrachloride. The results were remarkable; E15 not only decreased fibrosis and collagen deposition, but also improved liver function without the negative side effect of hypercalcemia, which is often associated with traditional VDR agonists.
These findings suggest that E15 could be a powerful and safer alternative for addressing liver fibrosis, highlighting the significant therapeutic potential of targeting the vitamin D receptor in liver diseases.
Our findings revealed that a high-fat diet led to vitamin D deficiency, insulin resistance, and a notable increase in liver weight. This also resulted in elevated liver enzymes and triglyceride levels, contributing to steatohepatitis, a concerning liver condition. When we introduced vitamin D supplementation, we observed a significant recovery in liver weight and overall improvement in liver health. The treatment also lowered harmful enzymes and triglycerides while helping control markers related to inflammation and fibrosis.
This study highlights that vitamin D supplementation can positively impact liver health in cases linked to obesity, offering an accessible and potentially effective strategy for addressing NAFLD. Notably, we found no adverse effects from the vitamin D treatment, suggesting it could be a safe option for individuals at risk.
Throughout the study, we assessed key health markers before and after supplementation, including liver function tests, lipid profiles, and glycaemic indices such as fasting blood glucose and insulin resistance. By the end of the trial, our findings indicated that vitamin D supplementation significantly improved fasting blood glucose levels and insulin resistance in the participants.
Specifically, we observed noteworthy increases in serum 25-hydroxy-vitamin D levels and reductions in fasting blood glucose and insulin resistance indicators. These results suggest that vitamin D might be an important player in improving metabolic health for those suffering from liver cirrhosis.
Through a combination of laboratory and animal studies, we assessed the expression of VDR in bile duct cells from pediatric patients, noting its connection to cholangitis rates after treatment. We discovered that activating VDR with vitamin D3 significantly reduced cell damage and apoptosis, which is the process of programmed cell death that can worsen BA.
We found that vitamin D3 helped mitigate viral-induced inflammation and cell death through specific cellular pathways, including one called the PLA2/PKC/ERK pathway. This suggests that vitamin D could be a valuable therapeutic option in managing liver diseases like BA, potentially offering new avenues for treatment and patient care.
Our findings revealed that vitamin D not only helped reduce body weight and improve liver health, but it also played a role in restoring normal metabolic functions. By reducing inflammation and protecting liver cells from damage, vitamin D enhanced insulin sensitivity and affected fat metabolism positively.
Notably, we found that vitamin D helped inhibit a harmful process known as ferroptosis—a type of cell death linked to liver injury. Through various assays, we confirmed that vitamin D treatment boosted the liver's antioxidant capabilities and lessened iron buildup in liver cells. Overall, our research suggests that vitamin D could be a promising therapeutic option for individuals suffering from MAFLD.
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Frequently Asked Questions
Liver disease encompasses a variety of conditions that affect the liver's ability to function effectively. The liver is a vital organ responsible for many important tasks, including metabolizing nutrients, detoxifying harmful substances, and producing bile for digestion. Common forms of liver disease include hepatitis, fatty liver disease, cirrhosis, and liver cancer. Each of these conditions can significantly impact liver function and overall health, leading to symptoms that range from fatigue and jaundice to more serious complications requiring urgent medical attention.
The causes of liver disease are diverse and can include chronic alcohol abuse, viral infections, autoimmune disorders, and metabolic conditions like obesity and diabetes. Early detection is key to managing liver disease effectively, often involving lifestyle changes, medications, and sometimes surgical interventions. Regular check-ups and liver function tests are recommended for individuals at higher risk, such as those with a family history of liver disease or those who lead certain lifestyle habits. Adopting a balanced diet and reducing alcohol intake can greatly aid in liver health and help prevent the onset of these conditions.
Vitamin D is a fat-soluble vitamin that's essential for maintaining healthy bones and teeth, supporting immune system function, and facilitating normal cell growth and development. It plays a crucial role in calcium absorption in the gut, which is vital for bone health. Unlike most vitamins, our bodies can produce Vitamin D when exposed to sunlight, specifically UVB rays, which is why it’s often referred to as the "sunshine vitamin." However, depending on your geographical location, lifestyle, and skin type, getting sufficient Vitamin D from the sun alone can be challenging, particularly during the winter months.
In addition to sunlight, Vitamin D can be obtained from certain foods such as fatty fish (like salmon and mackerel), fish liver oils, and fortified foods like milk and cereals. Some individuals may also consider supplements, especially if they're at risk for deficiency. Insufficient vitamin D levels are linked to various health issues, including rickets in children, osteomalacia in adults, and even an increased risk of chronic diseases. Regularly checking your vitamin D levels and consulting with a healthcare professional can help ensure you're meeting your needs for optimal health.
Recent studies have suggested that Vitamin D may play a beneficial role in liver health, especially in conditions such as non-alcoholic fatty liver disease (NAFLD) and hepatitis. Vitamin D is known for its anti-inflammatory and immunomodulatory properties, which could help mitigate some of the effects of liver disease. Observational studies have shown that individuals with liver disease often have lower levels of Vitamin D, and some research indicates that supplementation might improve liver function tests and overall health in these patients.
However, it's important to note that while there is promising research, Vitamin D should not be seen as a standalone treatment for liver diseases. Consultation with a healthcare provider is crucial to assess individual needs and to determine an appropriate treatment plan. More extensive clinical trials are needed to fully understand the implications of Vitamin D on liver health, including optimal dosing and timing for supplementation.
When it comes to noticing improvements from vitamin D supplementation, user experiences can vary significantly. Many users report seeing benefits within a few weeks to several months, depending on their individual health conditions and deficiencies. For instance, one user mentioned experiencing a significant reduction in joint pain just two weeks after starting vitamin D3, while another noted substantial improvement in vitamin D levels after six months of consistent supplementation (Read Review) (Read Review).
Specifically for those dealing with liver disease, some users have highlighted the importance of vitamin D in maintaining overall health and its potential role in recovery (Read Review). This aligns with the general consensus that persistence in supplementation—ranging from 2000 IU to higher doses—can lead to measurable improvements in both liver function and overall wellbeing over a few months. As always, it is advisable to consult with a healthcare professional before starting any new supplement regimen.
The scientific research surrounding Vitamin D supplementation suggests that it could play a beneficial role in managing various liver diseases. Studies indicate that Vitamin D can positively impact conditions like non-alcoholic fatty liver disease (NAFLD) and cirrhosis. For instance, one study demonstrated that Vitamin D supplementation improved liver health in obese mice with NAFLD, leading to reduced liver weight and improved metabolic markers [1]. Similarly, research involving cirrhosis patients showed significant improvements in insulin resistance and glucose levels following Vitamin D3 supplementation [17].
Moreover, Vitamin D's influence extends to liver fibrosis, where compounds targeting the Vitamin D receptor have shown promise in reducing this condition [8]. In pediatric studies, Vitamin D3 has been associated with protection against liver damage due to viral infections, indicating its potential therapeutic benefits in a variety of contexts [18]. Overall, while the evidence supporting Vitamin D's role in liver health is promising, further research is essential to solidify these findings and better understand dosage and treatment protocols.
According to user reviews, a variety of notable improvements in symptoms associated with vitamin D supplementation have been reported. Many individuals dealing with chronic conditions, such as rheumatoid arthritis and osteopenia, have experienced significant reductions in pain and inflammation. One user with rheumatoid arthritis noted a considerable decrease in joint inflammation and pain shortly after beginning NOW Foods vitamin D-3 (Read Review). Another user with osteopenia observed a marked improvement in their vitamin D levels after six months, which they attribute to their ongoing supplementation (Read Review).
In addition to physical alleviations, several users have reported enhanced immune function and overall vitality as a result of regular vitamin D intake. One user described feeling healthier and experiencing fewer illnesses since improving their vitamin D levels, emphasizing a notable boost to their immune defense (Read Review). Furthermore, those with respiratory issues have reported positive outcomes, with some mentioning that vitamin D helped manage bronchial asthma symptoms and assisted in recovery from viral infections, such as COVID-19 (Read Review) (Read Review). These anecdotal experiences suggest that vitamin D can be a beneficial supplement, though individual results will inevitably vary.
Based on user reviews, there appears to be a consensus that combining vitamin D supplementation with other health measures can offer benefits to those dealing with liver disease. Many users assert the significance of maintaining adequate vitamin D levels for overall recovery and liver health. For instance, one user noted that their liver disease is potentially linked to vitamin D deficiency, and they experienced enhanced well-being when taking 2000 IU daily (Read Review). Another user reinforced this by discussing how regular intake of vitamin D3 has been crucial for their immune system and overall health, particularly with liver health in mind (Read Review).
However, it is important to note that some users caution against high dosages, as excessive intake could lead to negative health outcomes, particularly concerning liver function (Read Review). As seen in other reviews, vitamin D supplementation seems to be usually coupled with a thoughtful approach to other supplements and general health strategies, indicating a collaborative effect on improving symptoms related to liver disease. Always consult a healthcare professional for personalized advice before commencing a new supplementation regimen.
Users report varying doses of Vitamin D, with many finding 2000 IU (50 micrograms) to be effective for managing health conditions, including liver disease. One user, who struggled with liver issues, noted significant health improvements after using 2000 IU and appreciated its suitability for their needs (Read Review). Another user, who was advised by their doctor due to a severe deficiency and associated liver disease, also reported a daily intake of 2000 IU as beneficial for their overall well-being and recovery (Read Review).
Additionally, some users recommend a range of 1500 to 5000 IU, depending on individual health needs and seasonal variations, such as increased intake during winter months (Read Review). While many users advocate for a regular dose of Vitamin D to support immune function and overall health, caution is warranted as higher doses over 4000 IU daily can lead to risks, particularly concerning liver health (Read Review). Therefore, it is prudent for individuals, especially those with liver disease, to consult healthcare professionals for appropriate dosing.
Our findings revealed that a high-fat diet led to vitamin D deficiency, insulin resistance, and a notable increase in liver weight. This also resulted in elevated liver enzymes and triglyceride levels, contributing to steatohepatitis, a concerning liver condition. When we introduced vitamin D supplementation, we observed a significant recovery in liver weight and overall improvement in liver health. The treatment also lowered harmful enzymes and triglycerides while helping control markers related to inflammation and fibrosis.
This study highlights that vitamin D supplementation can positively impact liver health in cases linked to obesity, offering an accessible and potentially effective strategy for addressing NAFLD. Notably, we found no adverse effects from the vitamin D treatment, suggesting it could be a safe option for individuals at risk.
After the 12-week period, we observed significant changes among those taking vitamin D. The serum levels of 25-hydroxy-vitamin-D3 increased substantially, alongside notable improvements in fasting blood glucose and insulin resistance, measured by HOMA-IR. These results suggest that vitamin D3 could play a beneficial role in managing certain metabolic aspects of liver disease in cirrhosis patients.
Overall, our study highlights the potential of vitamin D3 supplementation as a simple yet effective strategy to improve specific health parameters in people living with cirrhosis, paving the way for further exploration in this important area of research.
Our research found that more than a third of these novel compounds displayed strong affinity for VDR and showed the ability to activate it. Among these, one compound, E15, stood out as particularly effective. It significantly inhibited the activation of hepatic stellate cells (HSCs), which play a critical role in the progression of liver fibrosis, thereby reducing the production of harmful extracellular matrix components.
Encouraged by these promising in vitro results, we proceeded to test E15 in a mouse model of liver fibrosis induced by carbon tetrachloride. The results were remarkable; E15 not only decreased fibrosis and collagen deposition, but also improved liver function without the negative side effect of hypercalcemia, which is often associated with traditional VDR agonists.
These findings suggest that E15 could be a powerful and safer alternative for addressing liver fibrosis, highlighting the significant therapeutic potential of targeting the vitamin D receptor in liver diseases.
We also observed how VDR activators could mitigate damage caused by double-stranded RNA viruses. Through in vitro and in vivo experiments, we found that treatment with vitamin D3 reduced cell injury and apoptosis. Specifically, vitamin D3 worked by inhibiting autophagy, a process that can contribute to cell damage in this context.
Overall, we’ve highlighted that the 1,25-VD3/VDR/Src axis plays a significant role in protecting BECs from damage, promoting healthier liver function. Our findings suggest that vitamin D3 has therapeutic potential worth considering in the treatment of liver diseases related to cholangitis and other viral challenges.
References
- Chung SI, Liang L, Han H, Park KH, Lee JH, et al. Vitamin D Attenuates Non-Alcoholic Fatty Liver Disease in High-Fat Diet-Induced Obesity Murine Model. Yonsei Med J. 2025;66:75. doi:10.3349/ymj.2024.0038
- Derogar Kasmaei SR, Parastouei K, Hosseini Ahangar B, Saberifiroozi M, Taghdir M. Effects of vitamin D supplementation on the glycaemic indices, lipid profile and liver function tests in patients with cirrhosis: a double-blind randomised controlled trial. BMJ Nutr Prev Health. 2024;7:e000938. doi:10.1136/bmjnph-2024-000938
- Liu N, Zhao P, Cao P, Hui J, Pan Y, et al. Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell damage by inhibiting autophagy. BMC Gastroenterol. 2025;25:44. doi:10.1186/s12876-025-03640-5
- Zou C, Liu X, He M, Sun Y, Sang Y, et al. Insulin Resistance Mediates the Association Between Vitamin D and Non-Alcoholic Fatty Liver Disease. Int J Prev Med. 2024;15:77. doi:10.4103/ijpvm.ijpvm_221_23
- Diaz-Ruiz R, Poca M, Roman E, Panadero-Gomez R, Cuyàs B, et al. Vitamin D Supplementation Is Associated with Inflammation Amelioration and Cognitive Improvement in Decompensated Patients with Cirrhosis. Nutrients. 2025;17. doi:10.3390/nu17020226
- Wang Y, Jin J, Chen S, Shen Y. Modulation of magnesium intake on the association between vitamin D deficiency and severe hepatic steatosis in overweight and obese individuals. Magnes Res. 2024;37:58. doi:10.1684/mrh.2024.0536
- Jiang R, Lu M, Hua Y, Hong Z. Association between serum vitamin D and depression among non-alcoholic fatty liver disease. Asia Pac J Clin Nutr. 2025;34:112. doi:10.6133/apjcn.202502_34(1).0011
- Gao F, Guan C, Cheng N, Liu Y, Wu Y, et al. Design, synthesis, and anti-liver fibrosis activity of novel non-steroidal vitamin D receptor agonists based on open-ring steroid scaffold. Eur J Med Chem. 2025;286:117250. doi:10.1016/j.ejmech.2025.117250
- Biswas SA, Rukunuzzaman M, Biswas RK, Rahman SMH, Alam MS. Serum Vitamin D Status in Infants with Cholestatic Jaundice. Mymensingh Med J. 2025;34:192.
- Munoli AS, Mantur PG, Jalawadi VM. Child-Pugh Score and Vitamin D: Exploring a New Frontier in Liver Cirrhosis Assessment. Cureus. 2024;16:e74738. doi:10.7759/cureus.74738
- Liang Y, Jiang X, Zhao X, Tang T, Fan X, et al. Vitamin D alleviates HFD-induced hepatic fibrosis by inhibiting DNMT1 to affect the TGFβ1/Smad3 pathway. iScience. 2024;27:111262. doi:10.1016/j.isci.2024.111262
- Miao Y, Jiang Z, Song H, Zhang Y, Chen H, et al. Vitamin D supplementation alleviates high fat diet-induced metabolic associated fatty liver disease by inhibiting ferroptosis pathway. Eur J Nutr. 2024;64:50. doi:10.1007/s00394-024-03554-0
- Huang N, Su X, Yu T, Wu X, Lu B, et al. Serum 25-hydroxy vitamin D level is associated with elastography-detected liver fibrosis in patients with type 2 diabetes mellitus in China. Front Endocrinol (Lausanne). 2024;15:1420088. doi:10.3389/fendo.2024.1420088
- Johnson CD, Stevens CM, Bennett MR, Litch AB, Rodrigue EM, et al. The Role of Vitamin D Deficiency in Hepatic Encephalopathy: A Review of Pathophysiology, Clinical Outcomes, and Therapeutic Potential. Nutrients. 2024;16. doi:10.3390/nu16234007
- Morsy MA, Abdel-Latif R, Ibrahim MF, Marey H, Abdel-Gaber SA. Calcitriol ameliorates cisplatin-induced hepatorenal toxicity via regulation of Nrf2-Mrp2/p38 MAPK signaling in mice. Int J Immunopathol Pharmacol. 2024;38:3946320241306276. doi:10.1177/03946320241306276
- Luo WJ, Dong XW, Ye H, Zhao QS, Zhang QB, et al. Vitamin D 1,25-Dihydroxyvitamin D reduces lipid accumulation in hepatocytes by inhibiting M1 macrophage polarization. World J Gastrointest Oncol. 2024;16:4685. doi:10.4251/wjgo.v16.i12.4685
- Derogar Kasmaei SR, Parastouei K, Hosseini Ahangar B, Saberifiroozi M, Taghdir M. Effects of vitamin D supplementation on the glycaemic indices, lipid profile and liver function tests in patients with cirrhosis: a double-blind randomised controlled trial. BMJ Nutr Prev Health. 2024;7:e000938. doi:10.1136/bmjnph-2024-000938
- Liu N, Zhao P, Cao P, Hui J, Pan Y, et al. Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell damage by inhibiting autophagy. BMC Gastroenterol. 2025;25:44. doi:10.1186/s12876-025-03640-5
- Miao Y, Jiang Z, Song H, Zhang Y, Chen H, et al. Vitamin D supplementation alleviates high fat diet-induced metabolic associated fatty liver disease by inhibiting ferroptosis pathway. Eur J Nutr. 2024;64:50. doi:10.1007/s00394-024-03554-0
- Morsy MA, Abdel-Latif R, Ibrahim MF, Marey H, Abdel-Gaber SA. Calcitriol ameliorates cisplatin-induced hepatorenal toxicity via regulation of Nrf2-Mrp2/p38 MAPK signaling in mice. Int J Immunopathol Pharmacol. 2024;38:3946320241306276. doi:10.1177/03946320241306276
- Luo WJ, Dong XW, Ye H, Zhao QS, Zhang QB, et al. Vitamin D 1,25-Dihydroxyvitamin D reduces lipid accumulation in hepatocytes by inhibiting M1 macrophage polarization. World J Gastrointest Oncol. 2024;16:4685. doi:10.4251/wjgo.v16.i12.4685
- Kilani Y, Alsakarneh S, Madi MY, Mosquera DAG, Ferreira MN, et al. Autoimmune Hepatitis and Vitamin D Deficiency: A Nationwide Perspective. Aliment Pharmacol Ther. 2025;61:682. doi:10.1111/apt.18438
- Dai J, Song J, Chen X, Ding F, Ding Y, et al. 1,25(OH)D-treated mouse bone marrow-derived dendritic cells alleviate autoimmune hepatitis in mice by improving TFR/TFH imbalance. Immunopharmacol Immunotoxicol. 2025;47:59. doi:10.1080/08923973.2024.2435314
- Yaribeygi H, Ramezani M, Katsiki N, Mirmohammadkhani M, Tabaei NS. Efficacy of Adding Sitagliptin to Ongoing Metformin on Metabolic Profile, Triglyceride-Glucose Index, Vitamin D3, and Liver Tests in Patients Type 2 Diabetes Mellitus and Nonalcoholic Fatty Liver Disease: A Double-Blind Randomized Clinical Trial. Curr Ther Res Clin Exp. 2024;101:100764. doi:10.1016/j.curtheres.2024.100764
- Farrash WF, Idris S, Elzubier ME, Khidir EBA, Aslam A, et al. Enhanced hepatoprotective effects of empagliflozin and vitamin D dual therapy against metabolic dysfunction-associated steatohepatitis in mice by boosted modulation of metabolic, oxidative stress, and inflammatory pathways. Int J Exp Pathol. 2024;105:219. doi:10.1111/iep.12519
- Dharshan SS, Ramamurthy K, Kaliraj S, Manikandan K, Chitra V, et al. Combined effects of vitamin D3 and dioxopiperidinamide derivative on lipid homeostasis, inflammatory pathways, and redox imbalance in non-alcoholic fatty liver disease in vivo zebrafish model. Biotechnol Appl Biochem. 2024. doi:10.1002/bab.2666
- Fogacci F, Giovannini M, Di Micoli V, Grandi E, Borghi C, et al. Effect of Supplementation of a Butyrate-Based Formula in Individuals with Liver Steatosis and Metabolic Syndrome: A Randomized Double-Blind Placebo-Controlled Clinical Trial. Nutrients. 2024;16. doi:10.3390/nu16152454
- Abdel-Hamid GR, Mostafa DM, Fathy RM, Lotfy DM, Osman S. Cytokine storm modulation using cholecalciferol and low dose gamma radiation in Escherichia coli infected mice. Cell Biochem Funct. 2024;42:e4026. doi:10.1002/cbf.4026
- Yang A, Chen Y, Gao Y, Lv Q, Li Y, et al. Vitamin D exacerbates steatosis while calcipotriol inhibits inflammation in non-alcoholic fatty liver disease in knockout mice: a comparative study of two forms of vitamin D. Food Funct. 2024;15:4614. doi:10.1039/d4fo00215f
- Lu Y, Chen H, Chen Y, Zhao L, Hou S. Accumulated LPS induced by colitis altered the activities of vitamin D-metabolizing hydroxylases and decreased the generation of 25-hydroxyvitamin D. Chem Biol Interact. 2024;395:110997. doi:10.1016/j.cbi.2024.110997
- Lee SB, Jin MH, Yoon JH. The contribution of vitamin D insufficiency to the onset of steatotic liver disease among individuals with metabolic dysfunction. Sci Rep. 2024;14:6714. doi:10.1038/s41598-024-57380-9
- Guo E, Yuan H, Li R, Yang J, Liu S, et al. Calcitriol ameliorates the progression of hepatic fibrosis through autophagy-related gene 16-like 1-mediated autophagy. Am J Med Sci. 2024;367:382. doi:10.1016/j.amjms.2024.02.010
