bims-vitmet Biomed News
on Vitamin metabolism
Issue of 2025–09–28
eight papers selected by
Onurkan Karabulut, Berkeley City College
  1. In D-fence of vitamin D sufficiency- A perspective.
  2. Vitamins, Vascular Health and Disease.
  3. Vitamin D3 alleviates AD-like pathology in APP/PS1 mice by inhibiting pyroptosis and neuroinflammation via DJ-1/PARK7.
  4. Correction: Vitamin D status in post-medieval Northern England: Insights from dental histology and enamel peptide analysis at Coach Lane, North Shields (AD 1711-1857).
  5. VDR activation ameliorates intermittent hypoxia-related cognitive impairment by upregulating TREM2 transcription.
  6. Tocopherols and tocotrienols. A molecular dynamics study.
  7. Water-Soluble Vitamins (Riboflavin, Niacin, Pantothenic Acid) in Dogs with Chronic Liver Disease vs. Healthy Controls.
  8. Vitamin C Selectively Inhibits Kidney Renal Clear Cell Carcinoma Cell Growth by Suppressing the HIF-1 Pathway.
  1. Bone. 2025 Sep 22. pii: S8756-3282(25)00269-8. [Epub ahead of print]201 117657
    In D-fence of vitamin D sufficiency- A perspective.
    Sarah C Brennan, Jenny E Gunton, Arthur D Conigrave, Rebecca S Mason, Christian M Girgis.
      Vitamin D is well-established in its essential role in maintaining bone health. In recent years, however, researchers have explored potential influences of vitamin D on extra-skeletal functions, with vitamin D deficiency being implicated in several acute and chronic illnesses. Thus, large-scale randomised controlled trials (RCTs) have investigated the impact of vitamin D supplements on conditions including cardiovascular disease, diabetes, sarcopenia, frailty, and even some cancers. In this perspective, we weigh the evidence from these recent trials, drawing a cohesive understanding of vitamin D's potentially diverse effects. Limitations of the field and possible future directions of vitamin D research are considered, along with a discussion of the utility of repetitive vitamin D testing and supplementation for many of these conditions.
    Keywords:  Bone health; Chronic disease prevention; Extra-skeletal effects; Randomised controlled trials; Vitamin D
    DOI:  https://doi.org/10.1016/j.bone.2025.117657
  2. Nutrients. 2025 Sep 15. pii: 2955. [Epub ahead of print]17(18):
    Vitamins, Vascular Health and Disease.
    George Ayoub.
      Vascular health relies on the proper function of endothelial cells, which regulate vascular tone, blood fluidity, and barrier integrity. Endothelial dysfunction, often aggravated by inadequate vitamin absorption, contributes to a spectrum of clinical disorders, including cardiovascular disease, cerebrovascular disease, peripheral artery disease, age-related macular degeneration, lymphedema, and chronic venous insufficiency. B-group vitamins (especially folate, or vitamin B9), along with vitamins B12, B6, C, D, and E, are essential in maintaining endothelial function, supporting DNA synthesis, regulating methylation, enhancing cellular repair, mitigating oxidative stress and inflammatory signaling, and curtailing vascular damage. Folate is noted for its central function in one-carbon metabolism and in converting homocysteine to methionine, thereby reducing vascular toxicity. We cover natural dietary sources of folate, synthetic folic acid, and the biologically active forms 5-methyl-(6S)-tetrahydrofolate (L-5-MTHF, L-methylfolate) and 5-formyl-(6S)-tetrahydrofolate (levoleucovorin). Therapeutic strategies to address vascular health and prevent hyperhomocysteinemia in order to preclude follow-on disorders include targeted vitamin supplementation, dietary improvements to ensure a sufficient intake of bioavailable nutrient forms, and, in certain clinical contexts, the use of active L-methylfolate or levoleucovorin (a drug product) to bypass metabolic conversion issues. These evidence-based interventions aim to restore endothelial homeostasis, slow disease progression, and improve patient outcomes across a variety of disorders linked to poor vascular health.
    Keywords:  ASD; autism; cognitive decline; dementia; endothelium; folate; folate receptor autoantibody; homocysteine; lymphedema
    DOI:  https://doi.org/10.3390/nu17182955
  3. Neurosci Lett. 2025 Sep 21. pii: S0304-3940(25)00274-5. [Epub ahead of print] 138385
    Vitamin D3 alleviates AD-like pathology in APP/PS1 mice by inhibiting pyroptosis and neuroinflammation via DJ-1/PARK7.
    Chunyu Zhou, Yulin Wang, Longfei Zuo, Yufan Miao, Wenjie Li, Xing Li, Yuan Xue, Mengxin Li.
      Alzheimer's disease (AD) is the most common primary progressive neurodegenerative disorder, with inflammatory responses involved in its onset and progression. Vitamin D (VD) is known for its health benefits, including antioxidant effects. Recently, Deglycase protein 1 (DJ-1/PARK7) has been shown to potentially regulate in antioxidant activity and inflammation regulation. In this study, we investigated the therapeutic effects of VD3 (30 IU/g/w) in Dj-1 knockdown APPswe/PS1E9 (APP/PS1) mice. Pathological changes were assessed using the Morris water maze and Barnes maze, as well as immunofluorescence, thioflavin S staining, Nissl staining, TUNEL staining, Western blot, and RT-PCR. The results demonstrated that VD3 significantly ameliorated cognitive deficits and attenuated AD-like pathology in APP/PS1 mice. Moreover, VD3 upregulated DJ-1 expression and suppressed neuroinflammation and neuronal pyroptosis by modulating the NF-κB/NLRP3/caspase-1 and caspase-3/GSDME signaling pathways. Collectively, these findings suggest that DJ-1 mediate these protective effects, as its knockdown reversed VD3-induced improvements in neuroinflammation and neuronal pyroptosis, implicating that DJ-1 is a crucial modulator in the effects of VD3 on Alzheimer's disease pathology.
    Keywords:  AD-like Pathology; Alzheimer’s disease; DJ-1; Pyroptosis; Vitamin D
    DOI:  https://doi.org/10.1016/j.neulet.2025.138385
  4. PLoS One. 2025 ;20(9): e0333161
    Correction: Vitamin D status in post-medieval Northern England: Insights from dental histology and enamel peptide analysis at Coach Lane, North Shields (AD 1711-1857).
    Anne Marie E Snoddy, Heidi Shaw, Sophie Newman, Justyna J Miszkiewicz, Nicolas A Stewart, Tina Jakob, Hallie Buckley, Anwen Caffell, Rebecca Gowland.
      [This corrects the article DOI: 10.1371/journal.pone.0296203.].
    DOI:  https://doi.org/10.1371/journal.pone.0333161
  5. Int Immunopharmacol. 2025 Sep 23. pii: S1567-5769(25)01534-6. [Epub ahead of print]166 115543
    VDR activation ameliorates intermittent hypoxia-related cognitive impairment by upregulating TREM2 transcription.
    Jiahuan Xu, Hongyu Jin, Hui Shen, Hong Huang, Lujia Zhang, Yutong Wu, Ying Zou, Wei Wang, Wenyang Li.
      Neuroinflammation induced by intermittent hypoxia (IH) plays an essential role in the cognitive impairment associated with obstructive sleep apnea (OSA). It has been reported that the activation of Vitamin D receptor (VDR) can alleviate the neuroinflammation and neuronal injury in some neurodegenerative diseases However, it remains unknown whether VDR can play a similar role in OSA-related cognitive impairment and how it works. This study found that activating VDR by calcitriol enhanced the expression of triggering receptor on myeloid cells 2 (TREM2), promoted microglia M2 polarization, further mitigated neuroinflammation and neuronal damage induced by IH in mice and in BV2 cells. These improvements were attenuated in BV2 cells exposed to IH with calcitriol when TREM2 was knockdown. To determine how VDR regulated the expression of TREM2, potential binding sites between VDR and TREM2 promoter were identified in HEK293T cells. These results indicated that the activation of VDR could ameliorate IH-induced cognitive impairment by binding to TREM2 promoter region and promoting the transcription of TREM2. This study provides a potential therapeutic target for cognitive impairment in patients with OSA.
    Keywords:  Cognitive impairment; Intermittent hypoxia; Neuroinflammation; Obstructive sleep apnea; Triggering receptor on myeloid cells 2; Vitamin D receptor
    DOI:  https://doi.org/10.1016/j.intimp.2025.115543
  6. Chem Phys Lipids. 2025 Sep 19. pii: S0009-3084(25)00077-5. [Epub ahead of print]272 105541
    Tocopherols and tocotrienols. A molecular dynamics study.
    José Villalaín.
      Vitamin E denotes a cluster of eight molecules, i.e., α-tocopherol, β-tocopherol, δ-tocopherol, γ-tocopherol, α-tocotrienol, β-tocotrienol, δ-tocotrienol and γ-tocotrienol, where the α-tocopherol isoform is the major form. Vitamin E is one of the natural most potent antioxidants and an indispensable molecule for human health, since its major function is the inhibition of free-radical lipid peroxidation propagation. Vitamin E has a lipophilic nature and localize in membranes and lipoproteins and could affect either both its biological properties or membrane structure. I have used molecular dynamics to know the position and orientation of these eight biomolecules in water and inside a biomembrane, besides finding any interactions with their lipidic components. When they are in the membrane, all molecules tend towards their most extended conformation, inserting well between the phospholipid hydrocarbon chains. Our data agree with the general consensus, i.e., the chromanol group is located near the oxygen atom of cholesterol, whereas its hydrophobic chain extends to the membrane middle. This does not prevent the existence of flip-flop between the two monolayers. Significantly, the tocopherol/tocotrienol molecules inside the membrane did not aggregate. Remarkable, α-tocopherol presented a relatively high diffusion coefficient when compared to the other molecules and the α-tocopherol transfer protein seems to be the most suitable for its transport and transfer to the membrane. Although in principle any tocopherol or tocotrienol could function as an antioxidant, nature has chosen α-tocopherol thanks to the sum of a series of very subtle characteristics.
    Keywords:  antioxidant; membrane; molecular dynamics; tocopherol; tocotrienol; vitamin E
    DOI:  https://doi.org/10.1016/j.chemphyslip.2025.105541
  7. Vet Sci. 2025 Sep 11. pii: 877. [Epub ahead of print]12(9):
    Water-Soluble Vitamins (Riboflavin, Niacin, Pantothenic Acid) in Dogs with Chronic Liver Disease vs. Healthy Controls.
    Verena Habermaass, Aurora Cogozzo, Francesco Bartoli, Valentina Vitelli, Rebecca Dini, Veronica Marchetti.
       BACKGROUND: Water-soluble vitamin deficiencies are common in human chronic liver disease (CLD) due to impaired metabolic pathways. Vitamins B2 (riboflavin), B3 (niacin), and B5 (pantothenic acid) assume critical roles in hepatic and lipid metabolism and may exert hepatoprotective effects. In canine CLD, data beyond cobalamin are sparse, and no guidelines currently endorse B-vitamin supplementation.
    METHODS: This case-control study analysed 66 stored serum samples from client-owned dogs with CLD and 50 from healthy blood-donor dogs. CLD diagnosis required persistent (>2 months) elevation of at least two liver enzymes (ALP, GGT, AST, ALT) and ultrasonographic evidence of CLD. Serum vitamin concentrations were quantified by LC-MS/MS (ng/mL).
    RESULTS: Vitamin B2 was significantly lower in CLD dogs versus controls (median 48.4 vs. 85.5 ng/mL; p = 0.002). No significant difference was observed in B3 levels (p = 0.25). Vitamin B5 concentrations were significantly higher in the CLD group (median 176.5 vs. 116.1 ng/mL; p = 0.003).
    CONCLUSIONS: Reduced B2 may reflect impaired hepatic processing or absorption in canine CLD. The presence of normal or elevated B3 and B5 may relate to alternative metabolic pathways. This constitutes the first study assessing B2, B3, and B5 in canine CLD, underscoring riboflavin's potential interest in CLD dogs.
    Keywords:  B2; B3; B5; canine chronic liver disease; canine hepatic disease; niacin; pantothenic acid; riboflavin; vitamins; water-soluble
    DOI:  https://doi.org/10.3390/vetsci12090877
  8. Onco Targets Ther. 2025 ;18 1069-1081
    Vitamin C Selectively Inhibits Kidney Renal Clear Cell Carcinoma Cell Growth by Suppressing the HIF-1 Pathway.
    Che Wang, Yaoyang Zhou, Yu Liang, Jue Pan, Jinyu Qiao, Lingbo Chen, Silin Liu, Jie Chen, Jin Wang, Xiao Sun, Jinlu Ma, Mengjiao Cai.
       Aim: To observe the effect of vitamin C on Kidney renal clear cell carcinoma (KIRC) and investigate its mechanism.
    Methods and Results: Firstly, 29 vitamin C direct target proteins (DPTs) were identified by Drug Bank 5.0, and the protein-protein interaction (PPI) network and signaling pathways of vitamin C DPTs were analyzed. The results showed that vitamin C was not only related to KIRC, but also to the HIF-1 pathway. Meanwhile, the top 300 highly expressed genes of KIRC were obtained by GEPIA. Next, We compared the genes of four vitamin C targets in the PPI network with highly expressed genes in KIRC. Interestingly, these common genes are also involved in HIF-1 pathway. Additionally, we utilized RNA-Seq technology to explore the differentially expressed genes in KIRC with vitamin C compared to those not intervened. We observed that these differentially expressed genes exhibited a close association with hypoxia. Finally, we observed the inhibitory effect of Vitamin C on KIRC by Cell Counting Kit-8 (CCK8) assay, real-time quantitative PCR, Western blotting, flow cytometry, and colony formation assay, and confirmed that Vitamin C inhibits the growth of KIRC cells through the HIF-1 pathway.
    Conclusion: Through bioinformatics analyses, we identified the molecular mechanism of vitamin C's role in KIRC and verified it through a series of experiments. Combined bioinformatics analysis will play an important role in future drug-disease interaction studies.
    Keywords:  HIF-1 signaling pathway; integrated bioinformatical analysis; kidney renal clear cell carcinoma; therapeutic target genes; vitamin C
    DOI:  https://doi.org/10.2147/OTT.S512698
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