bims-vitmet Biomed News
on Vitamin metabolism
Issue of 2025–10–12
six papers selected by
Onurkan Karabulut, Berkeley City College
  1. Short-term and long-term effects of vitamin D supplementation for preterm infants: a systematic review and meta-analysis.
  2. Perinatal vitamin A excess impacts vitamin A and lipid metabolism in rat offspring.
  3. Investigating genetic links of vitamin D metabolism pathway genes (CYP2R1, CYP27B1, CYP24A1, and DBP) in Multiple Sclerosis patients.
  4. The inhibitory impact of glutathione (GSH) and ascorbic acid (vitamin C) compounds on glucose-6-phosphate dehydrogenase (G6PD) enzyme purified from sheep liver.
  5. Association of Poor Vitamin K Status with Inflammation and Gut Microbiota in Hemodialysis Patients: A Cross-Sectional Study.
  6. The role of vitamin C in melanoma cell death via activation of cytochrome C and TNF-α protein expression.
  1. J Perinatol. 2025 Oct 07.
    Short-term and long-term effects of vitamin D supplementation for preterm infants: a systematic review and meta-analysis.
    Seung Hyun Shin, Hyun Jung Kim, Ju Sun Heo.
      Meta-analysis conducted to evaluate the effectiveness of high-dose (≥800 IU/day) and low-dose (<800 IU/day) vitamin D supplementation on preterm infants. Study quality was evaluated using the Revised Cochrane risk-of-bias tool 2 for randomized trials. 21 studies included 1130 infants. Regarding short-term (before 40 weeks' postmenstrual age [PMA] or at discharge) outcomes, high-dose vitamin D supplementation was associated with increased serum 25-hydroxyvitamin D (25[OH]D) levels (mean difference 15.62 [13.35-17.88]) and growth velocities, as well as decreased vitamin D deficiency (VDD), skeletal hypomineralization, and mortality. In the subgroup analysis of high-dose supplementation stratified by dosage, 800 IU/day significantly increased serum 25(OH)D levels (mean difference 13.99 [9.03-18.95]) and reduced the risk of VDD (risk difference -0.21 [-0.32 to -0.10]) compared to 400 IU/day, without increasing the risk of vitamin D excess. The long-term outcomes assessed after 40 weeks' PMA or at follow-up visits showed no significant differences in vitamin D status or neurodevelopmental outcomes between the high-dose and low-dose groups. The certainty of the evidence ranges from moderate to very low. High-dose vitamin D supplementation improved short-term outcomes by increasing serum 25(OH)D levels, promoting growth, and reducing mortality. Among the high-dose regimens, 800 IU/day appeared to be the most appropriate dose.
    DOI:  https://doi.org/10.1038/s41372-025-02440-9
  2. Sci Rep. 2025 Oct 07. 15(1): 34987
    Perinatal vitamin A excess impacts vitamin A and lipid metabolism in rat offspring.
    Angélique Berthomé, Tiffany Antoine, Laure Meiller, Roland Govers, Philippe Guichard, Charlotte Sabran, Teresa Gonzalez, Marion Nowicki, Claire Bordat, Patrick Borel, Michel Grino, Valérie Sauvinet, Emmanuelle Reboul.
      Vitamin A (VA) supplementation has been recommended for pregnant women at-risk of deficiency, and is widely applied to children under 5 in developing countries. We addressed the effect of excessive VA exposure during pregnancy, lactation and first weeks of life on VA, vitamin E and lipid metabolism in rat offspring. Sprague-Dawley female rats were fed either a 2300 IU.kg-1 VA diet (control diet) or a 9858 IU.kg-1 VA diet (vitamin A supplemented diet - VAS diet) and mated with males fed the control diet. Weanlings were fed the same diet as their mothers until they were 8 weeks old. Organs and adipose tissue were collected from half of the offspring after fasting. The other half was force-fed an oil-in-water emulsion containing retinyl palmitate and [1,1,1-13C3]triolein. VAS-fed female and male offspring displayed a significant accumulation of VA in the liver (18 and 32 times more retinyl esters than respective controls, p < 0.0001) and VAS-fed males exhibited higher plasma retinol concentrations (+ 42.8 ± 6.6% compared to control males, p = 0.0011). Fasting plasma triglyceride concentration was higher for both VAS-fed females and males (+ 44.6 ± 6.8%, p = 0.0007 and + 58.8 ± 20.2%, p = 0.0343, compared to their respective controls). Lipid absorption was increased in VAS-fed males (+ 60.9% of [1-13 C]oleate absorption at 1.5 h post-gavage, p < 0.0001). Overall, our data show that VA overexposure disbalances VA status and detrimentally impacts lipid metabolism in offspring.
    Keywords:  Bioavailability; Intestine, liver; Retinol; Retinyl esters; Vitamin A; [1-13C]oleate
    DOI:  https://doi.org/10.1038/s41598-025-18896-w
  3. PLoS One. 2025 ;20(10): e0333924
    Investigating genetic links of vitamin D metabolism pathway genes (CYP2R1, CYP27B1, CYP24A1, and DBP) in Multiple Sclerosis patients.
    Laith Al-Eitan, Asaad Ataa.
      Multiple sclerosis (MS) is believed to result from a complex interplay of behavioral, genetic, and environmental risk factors. Furthermore, some studies indicated that vitamin D deficiency is linked to the emergence of different diseases, including MS. This study aims to determine the genetic associations between vitamin D metabolism gene polymorphisms and MS susceptibility in the Jordanian community. A total of 388 samples (192 MS patients and 196 controls). Genotypes for CYP2R1 (rs10741657, rs12794714), CYP27B1 (rs10877012), CYP24A1 (rs2248359), and DBP (rs7041, rs4588) were determined by PCR/RFLP assay method. The study revealed a significant association with increased MS risk in SNPs rs10877012 (C/A, P = 0.0002) of the CYP27B1 gene and rs4588 (A/A, P = 0.04) of the DBP gene. Additionally, the haplotypes of the CYP2R1 gene revealed a significant association with MS patients and controls (GG, p = 1e-04; AA, p < 0.0001). Moreover, only a SNP rs4588 of the DBP gene has been significantly associated (P = 0.04) with a clinical phenotype of multiple sclerosis and vitamin D deficiency. Understanding these genetic variations in multiple sclerosis susceptibility genes can help healthcare professionals improve early diagnosis and develop personalized treatment options.
    DOI:  https://doi.org/10.1371/journal.pone.0333924
  4. Arch Physiol Biochem. 2025 Oct 07. 1-10
    The inhibitory impact of glutathione (GSH) and ascorbic acid (vitamin C) compounds on glucose-6-phosphate dehydrogenase (G6PD) enzyme purified from sheep liver.
    Zehra Bas, Vedat Turkoglu.
       OBJECTIVE: Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme with many essential biochemical functions. However, in various cancer diseases, increased activity of G6PD causes cancer cells to grow, so G6PD inhibitors have become a significant area of research in cancer treatment.
    MATERIALS AND METHODS: Here, G6PD was purified 4530-fold with affinity chromatography using 2',5'-ADP Sepharose 4B from sheep liver. The effects of reduced glutathione (GSH) and ascorbic acid (vitamin C) on G6PD activity were explored.
    RESULTS AND DISCUSSION: GSH and ascorbic acid showed a significant inhibitory effect on G6PD, and IC50 values were found as 0.37 µM and 34.66 µM, respectively. The inhibition type from Lineweaver-Burk plots of these compounds was identified as non-competitive inhibition. The Ki values of GSH and ascorbic acid were calculated as 0.48 µM and 30.47 µM, respectively.
    CONCLUSION: In this study, it was observed that GSH and ascorbic acid antioxidant compounds exhibit an inhibitory effect on G6PD and may be protective and preventive against cancer.
    Keywords:  Ascorbic acid (vitamin C); glucose-6-phosphate dehydrogenase (G6PD); inhibition; purification; reduced glutathione (GSH)
    DOI:  https://doi.org/10.1080/13813455.2025.2567343
  5. J Nutr Biochem. 2025 Oct 04. pii: S0955-2863(25)00301-8. [Epub ahead of print] 110139
    Association of Poor Vitamin K Status with Inflammation and Gut Microbiota in Hemodialysis Patients: A Cross-Sectional Study.
    Ligia Soares Lima, Marcia Ribeiro, Ludmila F M F Cardozo, Rudolf Bittner, Marcelo Ribeiro-Alves, Júnia Schultz, Alexandre Soares Rosado, Paulo Emilio Correa Leite, Lia S Nakao, Leon J Schurgers, Denise Mafra.
       BACKGROUND: Vitamin K insufficiency is common in chronic kidney disease (CKD) and may be associated with gut dysbiosis, which decreases the number of vitamin K-producing bacteria. This insufficient status worsens inflammation, leading to vascular calcification and oxidative stress.
    OBJECTIVE: This study investigates the correlation between vitamin K status and gut microbiota composition, and its association with inflammation in hemodialysis (HD) patients.
    METHODS: In this cross-sectional study, patients were grouped based on dephosphorylated-uncarboxylated matrix gla-protein (dp-ucMGP) levels: adequate (≤ 500 pmol/L) or inadequate (> 500 pmol/L) vitamin K status. Plasma cytokines were analyzed using a multiplex assay, and uremic toxins via reverse-phase high-performance liquid chromatography (RP-HPLC). Gut microbiota composition was assessed in a subgroup using fecal DNA extraction and 16S rRNA gene sequencing on the Illumina NovaSeq PE250 platform.
    RESULTS: Among 107 patients (53 [interquartile range = 16] years and 36 [interquartile range = 42] months on HD) completed the study, 70 patients (53 years, BMI, 24.2Kg/m2) exhibited insufficient vitamin K status, and 37 patients presented adequate status (52.5 years, BMI, 25.6Kg/m2). Patients with inadequate vitamin K status exhibited significantly higher levels of interleukin (IL)-6, IL-1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), and granulocyte colony-stimulating factor (G-CSF) compared to patients with adequate status, reflecting elevated inflammatory marker levels in patients with insufficient vitamin K. Additionally, Bacteroides, a key vitamin K2-producing genus, was decreased in patients with inadequate vitamin K status.
    CONCLUSIONS: Gut dysbiosis is a consequence of CKD, which can result in reduced production of vitamin K and subsequent insufficient status. Additionally, inadequate vitamin K status may contribute to the inflammatory state in patients undergoing HD.
    Keywords:  Chronic Kidney Disease; Gut Microbiota; Inflammation; Menaquinone; Renal Dialysis; Vitamin K
    DOI:  https://doi.org/10.1016/j.jnutbio.2025.110139
  6. Sci Rep. 2025 Oct 06. 15(1): 34733
    The role of vitamin C in melanoma cell death via activation of cytochrome C and TNF-α protein expression.
    Eva Krishna Sutedja, Tiara Rachmaputeri Arianto, Ghabrina Saraswati Elgianda, Endang Sutedja, Ronny Lesmana, Oki Suwarsa, Reti Hindritiani, Pati Aji Achdiat, Hendra Gunawan, Budi Setiabudiawan.
      This study investigates the effect of vitamin C on cytochrome c and TNF-α expression, representing intrinsic and extrinsic apoptotic pathways in B16-F10 melanoma cells. B16-F10 melanoma cells (ATCC® CRL-6475™) were treated with vitamin C for 12 and 24 h. Expression of cytochrome c, TNF-α, caspase-3, and caspase-9 proteins was evaluated using in-cell western (ICW) assay. RT-qPCR was used to assess gene expression of Caspase-8, IL-6, PARP-γ, and TGF-β1. Morphological signs of cell death appeared within 12 h. A significant increase in cytochrome c expression at 3,000 µM concentrations of vitamin C was observed (p = 0.002), along with increases at 3,500 µM (p = 0.023), 4,000 µM (p = 0.0001), and 5,000 µM (p = 0.0001). Caspase-3 expression significantly increased at 3,000 µM (p = 0.012) and 5,000 µM (p = 0.048), while caspase-9 was not significant. TNF-α expression also increased significantly from 3,000 to 5,000 µM (all p < 0.01). Caspase-8 and PARP-γ mRNA levels were upregulated at 3,000 and 5,000 µM (p < 0.05). IL-6 and TGF-β1 changes further supported apoptosis activation. Vitamin C induces apoptosis in B16-F10 melanoma cells via intrinsic and extrinsic pathways, particularly at 3,000 and 5,000 µM concentrations, as shown by cytochrome c, TNF-α, and caspase-3 expression.
    Keywords:  Apoptosis; Cytochrome c; Extrinsic pathway; Intrinsic pathway; TNF-α; Vitamin c
    DOI:  https://doi.org/10.1038/s41598-025-18372-5
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