bims-vitmet Biomed News
on Vitamin metabolism
Issue of 2025–10–05
six papers selected by
Onurkan Karabulut, Berkeley City College



  1. Nutr Metab (Lond). 2025 Oct 02. 22(1): 113
      Vitamin D (VD) is a pleiotropic secosteroid hormone with well-established roles in calcium homeostasis, bone metabolism, and emerging functions in immune regulation, inflammation, and chronic disease modulation. In this paper, we provide a comprehensive summary of the current research on the significance of VD for bone health, with emphasis on its mechanism of action and its clinical significance in bone health. This review starts with an overview of VD metabolism, with emphasis on the enzyme transformation of vitamin D3 (VD3) and vitamin D2 (VD2) into the active 1,25-dihydroxyvitamin D (1α,25(OH)2D) and their genomic and non-genomic signaling pathways through the Vitamin D receptor (VDR). Then, we discuss how VDR polymorphisms affect disease susceptibility and the dual role of VD in promoting innate immunity as well as inhibiting over-adaptive immunity. Our main focus is placed on VD's involvement in bone destruction diseases, including osteoarthritis (OA), osteoporosis (OP), rheumatoid arthritis (RA), and bone tuberculosis. For OA, there is conflicting evidence on whether VD supplementation reduces cartilage degradation or pain. In OP, vitamin D deficiency aggravates bone loss, but the effectiveness of supplementation is dependent on baseline and calcium supplementation. For RA, the immunomodulatory effects of VD may decrease the activity of the disease, whereas in tuberculosis, VD increases the clearance of macrophage-mediated mycobacterial clearance, although the clinical study data are still inconclusive. This review underscores VD as a critical mediator of bone-immune crosstalk while calling for rigorous translational research to clarify its therapeutic potential across diverse diseases.
    Keywords:  Bone destruction diseases; Immunoregulation; Vitamin D
    DOI:  https://doi.org/10.1186/s12986-025-01011-1
  2. Open Med (Wars). 2025 ;20(1): 20241086
       Background: Vitamin C is a key to many important functions. It stimulates the immune system by protecting humans from infections and shows notable anti-viral and anti-inflammatory properties. With the antioxidative properties it acts against free radicals and cellular aging and prevents tumors. It is also involved in the synthesis of collagen, a structural protein that is essential for the formation of connective tissue as epidermis, muscle, bone, cartilage, etc. Vitamin C promotes the absorption of iron contributing to the production of red blood cells and the synthesis of hemoglobin. Scurvy is a nutritional disorder caused by low vitamin C levels which manifests with varied symptoms affecting multiple organ systems. Vitamin C also known as l-ascorbic acid, is a water-soluble nutrient and is a necessary element as the humans are unable to synthesize it. Vitamin C has an important role in the biochemical reactions of connective tissue synthesis. Presenting manifestations include malaise, gingival bleeding, impaired wound healing, perifollicular hemorrhage, dry hair and brittle nails, iron deficiency, muscle and joint pain, pulmonary hypertension, and other symptoms. The persistent reduced supply of vitamin C in the absence of treatment is cause of a severe progressive worsening of the clinical conditions. The disorder is uncommonly reported in high social level countries and in mentally wellbeing children.
    Methods: Herewith, we report case-series of eight children with scurvy diagnosed in two Pediatric Hospitals in Catania, Italy "Policlinico G. Rodolico" and "Cannizzaro" in the last 2 years, October 2021-October 2023. In addition, a systematic literature review of 126 articles with 253 cases of scurvy including age, sex, main clinical manifestations, and eventual presence of neurodevelopmental disorders is reported. Main characteristic of vitamin C and negative effects of its lack with clinical manifestations, diagnosis, treatment, and prognosis are also referred.
    Results: Malnutrition, gastrointestinal, and neurological disorders, are the associated predisposing factors. In the present case-series, to the higher incidence of scurvy compared to others Italian Regions may have contributed an erroneous old prejudice of parents who refuse to give citrus fruits to young children as lemon and oranges may cause cystitis as well severe toxicity when mixed with milk.
    Conclusion: This study aims to alert on the scurvy as a possible cause of childhood disorder also in well industrialized regions, and to offer diagnostic tools for identifying subjects suffering from this illness.
    Keywords:  gingival bleeding; l-ascorbic acid; scurvy; swollen gum; vitamin C deficiency
    DOI:  https://doi.org/10.1515/med-2024-1086
  3. Database (Oxford). 2025 Jan 18. pii: baaf049. [Epub ahead of print]2025
      The importance of vitamin B12 (cobalamin) in numerous biological processes, including DNA synthesis and cellular energy production, underscores the need for therapeutic and public health strategies to address B12 insufficiency/deficiency in the population. Genetic variations in pathways influencing cobalamin absorption, transport, and metabolism can affect various direct and indirect measures of vitamin B12 status. To facilitate a structured approach to studying these genetic factors, we aimed to systematically curate and create a user-friendly web database that offers comprehensive data on genetic variants influencing B12 biomarkers. A PubMed search was performed for 5 B12 traits [total serum/plasma B12, holotranscobalamin (active B12), total transcobalamin, holohaptocorrin, and methylmalonic acid] resulting in 493 research publications, of which 47 relevant publications were reviewed further. The database backend was built using MongoDB and the web interface was coded in PHP, JavaScript, HTML, and CSS on an Apache HTTP server. We have manually curated and compiled the Cobalamin Associated Genetic Variant (CobVar) database, comprising a total of 324 genetic variant associations for 5 different vitamin B12 traits involving 222 unique genetic variants and 84 genes identified across several genome-wide association studies and candidate gene studies. About one-third of the total genetic variant associations have been reported in >1 independent studies and 15 variants in >1 ethnic group. FUT2 gene showed the maximum number of associations for total serum/plasma B12 (N = 39), followed by MTHFR (N = 24) and TCN2 (N = 23). The database is accessible online at https://datatools.sjri.res.in/VBG/. CobVar is a vital resource for researchers and nutritionists, offering quick access to the latest developments in B12-related genetic variant research and serves as a valuable tool for advancing personalized treatment. Database URL: https://datatools.sjri.res.in/VBG/.
    DOI:  https://doi.org/10.1093/database/baaf049
  4. Front Nutr. 2025 ;12 1611829
      Hepatocellular carcinoma (HCC) is one of the most common cancers globally, with nearly 1 million new cases diagnosed annually. It is a complex disease, with hepatitis B virus (HBV) and hepatitis C virus (HCV) infections being the most common etiological factors worldwide. Despite advances in therapy, survival rates for advanced and/or metastatic HCC remain low, with mortality rates 2.3 times higher in men than women. The liver's immune system typically maintains an anti-inflammatory environment, contributing to immune tolerance to exogenous, food-derived antigens. However, disruption of the balanced interplay between immune factors within the hepatic microenvironment-due to viral hepatitis, excessive alcohol intake, non-alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis (NASH)-can lead to chronic inflammation, oxidative stress, a cumulative mutational burden, cirrhosis, and eventually, malignant transformation. Once HCC is established, however, a functional pro-inflammatory immune response becomes critical to controlling tumor progression, as evidenced by the recent success of immune checkpoint inhibitor (ICI) treatments in HCC patients. In addition to ICIs, other novel immunotherapeutic intervention strategies, such as cancer vaccines and adoptive T cell therapies, are currently being investigated. Furthermore, adequate nutrition plays a critical role in modulating immune function, with vitamin D being a key nutrient for immune/regulation. In this review, we will discuss the potential role of vitamin D in HCC immunity and recent immunotherapeutic advances in the management of this malignancy.
    Keywords:  HCC; artificial intelligence; cancer; liver; technology; tumor microenvironment; vaccines; vitamin D
    DOI:  https://doi.org/10.3389/fnut.2025.1611829
  5. Front Cardiovasc Med. 2025 ;12 1626769
       Background: Stimulated by retinoic acid gene 6 (STRA6) is a cell surface receptor that regulates cellular uptake of vitamin A metabolites and cardiac development. We hypothesized that Stra6 expression attenuates ischemic injury-induced heart failure following myocardial infarction (MI) by vitamin A-dependent mechanisms.
    Methods: MI was induced in mice with Stra6 germline deletion, vitamin A deficiency (VitAD) by combined lecithin-retinol acyltransferase (Lrat) germline deletion and feeding with a vitamin A-deficient diet. Contractile function was determined by transthoracic echocardiography, cardiac structure was assessed by histological analysis, and gene profiling was performed by RNA sequencing.
    Results: Stra6 deletion and VitAD did not impact contractile function and cardiac structure under basal conditions. Stra6 deficiency resulted in myocardial rupture, with the majority of mice dying by 4 days post-MI, which additional VitAD attenuated. Interestingly, contractile function, mRNA expression of heart failure markers, and cardiac structure were not different between groups 3 days post-MI. Gene profiling 3 days post-MI revealed decreased Wnt signaling in Stra6-deficient relative to wildtype hearts, which was reversed by VitAD.
    Conclusion: The present study identifies an unexpected role for VitAD, which preserves Wnt signaling and attenuates cardiac rupture in Stra6-deficient hearts following ischemic injury.
    Keywords:  cardiac remodeling; heart failure; myocardial infarction; stimulated by retinoic acid gene 6; vitamin A; wnt signaling
    DOI:  https://doi.org/10.3389/fcvm.2025.1626769