bims-vitmet Biomed News
on Vitamin metabolism
Issue of 2025–05–18
seven papers selected by
Onurkan Karabulut, Berkeley City College
  1. Vitamin D status, vitamin D receptor polymorphisms, and risk of cardiometabolic multimorbidity.
  2. Nonlinear associations of serum vitamin D levels with advanced liver disease and mortality: a US Cohort Study.
  3. Nutritional Deficiencies and Reduced Bone Mineralization in Ulcerative Colitis.
  4. Dietary Vitamin C Intake Affects Lung Function Through White Blood Cell.
  5. Investigating nutrient intake during use of glucagon-like peptide-1 receptor agonist: a cross-sectional study.
  6. Role of vitamins in the development and treatment of osteoporosis (Review).
  7. High-dose vitamin C promotes mitochondrial biogenesis in HCT116 colorectal cancer cells by regulating the AMPK/PGC-1α signaling pathway.
  1. Nutr J. 2025 May 11. 24(1): 76
    Vitamin D status, vitamin D receptor polymorphisms, and risk of cardiometabolic multimorbidity.
    Jianhua Ma, Pingan Li, Jinqi Wang, Haiping Zhang, Zhiwei Li, Lixin Tao, Xinghua Yang, Yanxia Luo, Xiuhua Guo, Bo Gao.
       BACKGROUND: The prevalence of cardiometabolic multimorbidity (CMM) has increased substantially in recent years. Previous studies have established the associations between vitamin D, vitamin D receptor (VDR) polymorphisms, and the risk of individual cardiometabolic disease (CMD). However, the role of these factors in the progression of CMD to CMM or mortality remains unclear. This study aimed to investigate the associations between vitamin D, VDR polymorphisms, and the dynamic progression of CMM, as well as to explore the potential modification effect of VDR polymorphisms.
    METHODS: Data for this cohort study were extracted from the UK Biobank. CMM was defined as the coexistence of at least two CMDs, including type 2 diabetes (T2D), coronary heart disease (CHD), and stroke. A multi-state model was used to analyze associations between serum 25(OH)D, VDR polymorphisms and the dynamic progression of CMM.
    RESULTS: The sample included 396,192 participants. Over a median follow-up of 13.8 years, 55,772 individuals experienced at least one CMD and 28,624 died. Compared to participants with 25(OH)D < 25 nmol/L, those with 25(OH)D ≥ 75 nmol/L had HRs of 0.70 (95% CI, 0.67, 0.72) for baseline to first CMD (FCMD), 0.74 (95% CI, 0.67, 0.82) for FCMD to CMM, 0.66 (95% CI, 0.62, 0.70) for baseline to death, 0.84 (95% CI, 0.77, 0.92) for FCMD to death, and 0.85 (95% CI, 0.70, 1.03) for CMM to death. L-shaped relationships of these associations were noted, with a threshold around 45 nmol/L. The rs1544410 (BsmI) T alleles may have a detrimental effect, while the rs11568820 (Cdx2) T alleles may exert a protective effect in the early stages of CMM progression. Additionally, VDR polymorphisms significantly modified the association between serum 25(OH)D and certain stages of CMM progression.
    CONCLUSIONS: Maintaining adequate vitamin D levels, as a readily implementable intervention strategy, not only reduces the risk of initial CMD but also delays the progression to CMM or death. Risk stratification based on VDR polymorphisms provides further insights for developing personalized prevention strategies.
    Keywords:  Cardiometabolic Multimorbidity; Vitamin D; Vitamin D receptor polymorphisms
    DOI:  https://doi.org/10.1186/s12937-025-01139-z
  2. Therap Adv Gastroenterol. 2025 ;18 17562848251338669
    Nonlinear associations of serum vitamin D levels with advanced liver disease and mortality: a US Cohort Study.
    Yuan-Tsung Tseng, Chun-Hsiang Wang, Jung-Der Wang, Kow-Tong Chen, Chung-Yi Li.
       Background: Vitamin D deficiency is prevalent and linked to chronic diseases; its association with advanced liver disease progression requires clarification.
    Objectives: To investigate the association between vitamin D levels and risks of liver cirrhosis, hepatocellular carcinoma (HCC), and mortality, and assess risk changes after achieving sufficiency post-supplementation.
    Design: This was a retrospective cohort study.
    Methods: Utilized TriNetX US data (3,905,594 patients, 2000-2024). Adults with vitamin D deficiency (20.00-30.00 ng/mL) were compared with those with sufficient levels (30.01-80.00 ng/mL). Follow-up was initiated from the first vitamin D test or start of supplementation to minimize immortal time bias. Propensity score matching (1:1) balanced >20 baseline confounders.
    Results: After matching, 1,204,760 patients with vitamin D deficiency and 1,204,760 with sufficient vitamin D levels were included. Vitamin D deficiency was associated with an increased risk of liver cirrhosis (hazard ratio (HR), 1.30; 95% confidence interval (CI), 1.25-1.36), HCC (HR, 1.22; 95% CI, 1.08-1.37), and all-cause mortality (HR, 1.14; 95% CI, 1.13-1.16). Achieving sufficient vitamin D levels reduced the risk of all-cause mortality (HR, 0.93; 95% CI, 0.88-0.99) and aligned HCC outcomes (HR, 1.16; 95% CI, 0.68-2.00). However, it did not significantly reduce the risk of liver cirrhosis (HR, 2.05; 95% CI, 1.69-2.50). Dose-response analysis showed a U-shaped relationship for liver cirrhosis and HCC, with the lowest risks at 40-60 ng/mL.
    Conclusion: Serum vitamin D levels showed a nonlinear association with liver cirrhosis and HCC risk; deficiency independently increased the risks for cirrhosis, HCC, and mortality. Supplementation achieving sufficiency reduced mortality and normalized HCC risk but not cirrhosis risk, potentially reflecting limitations in reversing established disease. The lowest liver disease risk was associated with vitamin D levels of 40-60 ng/mL in this cohort, although causality and the clinical benefit of targeting this specific range require confirmation.
    Keywords:  hepatocellular carcinoma; liver cirrhosis; mortality; vitamin D deficiency; vitamin D supplementation
    DOI:  https://doi.org/10.1177/17562848251338669
  3. J Clin Med. 2025 May 06. pii: 3202. [Epub ahead of print]14(9):
    Nutritional Deficiencies and Reduced Bone Mineralization in Ulcerative Colitis.
    Filippo Vernia, Emanuela Ribichini, Giorgia Burrelli Scotti, Giovanni Latella.
      Background: Inadequate dietary intake of vitamin D, vitamin K, and calcium, as well as sub-optimal sunlight exposure, can lead to bone loss in the general population, and more so in patients with ulcerative colitis, who are burdened by additional predisposing factors for osteoporosis, such as chronic inflammation and cortisone use. However, micronutrient deficiencies, if present, are easily corrected by nutritional intervention. While the relation between calcium and vitamin D and bone metabolism is well known, fewer data are available for vitamin K, for both healthy individuals and patients. The aim of this review is to provide an overview of recent reports focusing on nutritional deficits relevant to the development of osteoporosis/osteopenia in patients affected by ulcerative colitis. Methods: A systematic electronic search of the English literature up to January 2025 was performed using Medline and the Cochrane Library. Results: Despite being central in bone mineralization, data on dietary calcium intake in ulcerative colitis are relatively scarce, deriving mostly from mixed inflammatory bowel disease cohorts. Although lower than controls, dietary calcium intake approaches the recommended daily allowance, which establishes the necessary daily intake of nutrients. Conversely, vitamin D and vitamin K deficiencies are highly prevalent in ulcerative colitis patients. The widely shared opinion that milk and lactose-containing foods, as well as vegetables, worsen diarrhea is a prime determinant of inadequate vitamin D and vitamin K intake. Conclusions: Increased awareness of the importance of nutrition and the common occurrence of nutritional deficits represents the first step for the development of dietary intervention strategies to counteract the increased risk of osteoporosis in ulcerative colitis patients.
    Keywords:  IBD; UC; calcium; deficiency; diet; inflammatory bowel diseases; nutrition; ulcerative colitis; vitamin D; vitamin K
    DOI:  https://doi.org/10.3390/jcm14093202
  4. Food Sci Nutr. 2025 May;13(5): e70299
    Dietary Vitamin C Intake Affects Lung Function Through White Blood Cell.
    Biao Hu, Lu Yuan, Yueyang Zhang, Weiling Deng, Haoyu Zhong, Chengyu Miao, Chudong Wang, Jiaxin Cai.
      As an antioxidant, vitamin C has been increasingly used in the treatment of various pulmonary diseases in recent years. However, the mechanism by which vitamin C affects lung function remains unclear to this day. Given its low cost and low risk, vitamin C is highly suitable for widespread use as a conventional treatment, making research into its mechanisms of influencing lung function necessary. Considering the potential association between vitamin C and white blood cells (WBCs), it may influence lung function by affecting white blood count (WBC). The potential impacts of WBCs on the lungs may include damage to the lung parenchyma through proteases released by these cells, as well as the effects of inflammatory factors on alveolar epithelial cells, among other mechanisms. This study aims to explore the potential relationship between dietary vitamin C intake, WBC, and lung function through a cross-sectional study. This cross-sectional study included data from 15,738 participants in the National Health and Nutrition Examination Survey (NHANES) from three time periods: 2007-2008, 2009-2010, and 2011-2012. Parallel mediation analysis was conducted using a multivariable logistic regression model to assess the relationships between dietary vitamin C intake, WBC, and lung function. Following the cross-sectional study, we further incorporated Mendelian randomization (MR) analysis to strengthen the validity of the findings. The results of this cross-sectional study showed that dietary vitamin C intake was negatively associated with WBC (p < 0.05, β < 0), while WBC was also negatively associated with lung function. In contrast, dietary vitamin C intake was positively associated with lung function, with a significant positive mediation effect (p < 0.05, β > 0). These findings suggest that vitamin C may influence lung function by modulating WBC levels. The study may reveal part of the mechanism through which vitamin C affects lung function, specifically through the mediation of WBC. The roles of inflammation and proteases could be potential underlying mechanisms. However, further research is required to clarify the biochemical mechanisms. This study provides a reference for the clinical use of vitamin C in the treatment of related pulmonary diseases and promotes further research into its broader effects.
    Keywords:  FEV1; FVC; WBC; cross‐sectional study; vitamin C
    DOI:  https://doi.org/10.1002/fsn3.70299
  5. Front Nutr. 2025 ;12 1566498
    Investigating nutrient intake during use of glucagon-like peptide-1 receptor agonist: a cross-sectional study.
    Brittany Johnson, Mary Milstead, Olena Thomas, Tyler McGlasson, Lauren Green, Rachel Kreider, Rachel Jones.
       Background: Glucagon-like peptide-1 receptor agonist (GLP-1RA) pharmaceutical interventions have advanced medical treatment for obesity, yet little is known about nutrient intake while using a GLP-1RA. The purpose of this study was to compare nutrient intake while using a GLP-1RA to the Dietary Reference Intakes (DRI).
    Methods: A cross-sectional study was conducted in a sample of participants who had been using GLP-1RA for at least one month (N = 69). Participants answered online survey questionnaires and completed a 3-day food record. Descriptive statistics (means, standard deviations) were calculated for all participant demographic characteristics and average 3-day nutrient intakes. Average 3-day nutrient intakes were compared to the DRI using 95% confidence intervals (CI). A Bonferroni correction applied accepted significance at p ≤ 0.00156. One-way ANOVA analysis was conducted to compare the self-reported MyPlate servings to recorded servings from the 3-day food record.
    Results: Compared to the DRI reference values, participants consumed adequate amounts of B-vitamins, copper, phosphorus, selenium, and zinc. Participants had insufficient intakes of several key nutrients below the DRI, including fiber (14.5 g; CI: 12-17), calcium (863 mg; CI: 756-970), iron (12.1 mg; CI: 11-13), magnesium (266 mg; CI: 236-297), potassium (2,186 mg; CI: 1,969-2,402), choline (305 mg; CI: 268-342), vitamin A (560 mcg RAE; CI: 469-651), vitamin C (51 mg; CI: 41-61), vitamin D (4 mcg; CI: 3-5), vitamin E (9.6 mg; CI: 8-11), and p < 0.00156. Participants overconsumed % calories from fat (39.9%; CI: 38, 42), and saturated fat (26 g; CI: 26, 26), p < 0.00156. Participants did not meet the daily recommended MyPlate servings for fruit, vegetables, grains, or dairy (p < 0.01). Protein intake (% total calories) was within the AMDR, however based on a g/kg/day, protein intake was significantly under daily needs.
    Conclusion: Participants on a GLP-1RA are not meeting the DRI for several vital nutrients through their diet or higher protein needs during weight loss. Patient-centered nutritional guidance is essential to optimize health outcomes and prevent unintended health consequences. Future large-scale studies are needed to assess the replicability of these findings and provide custom nutritional guidance for those on a GLP-1RA medication.
    Keywords:  diet; dietary reference intakes; glucagon-like peptide-1 receptor agonists; nutrient intake; nutrition; weight loss
    DOI:  https://doi.org/10.3389/fnut.2025.1566498
  6. Int J Mol Med. 2025 Jul;pii: 109. [Epub ahead of print]56(1):
    Role of vitamins in the development and treatment of osteoporosis (Review).
    Mingze Jiang, Genghan Li, Keda Yang, Lin Tao.
      Osteoporosis has escalated into a pressing public health challenge amidst global demographic aging. Conventional diagnostic approaches and therapeutic interventions demonstrate growing limitations in both risk stratification and epidemiological control. In this context, serological monitoring and targeted nutrient supplementation emerge as promising preventive strategies. Vitamins, fundamental regulators of cellular homeostasis, demonstrate particular significance in bone remodeling processes. The present comprehensive review elucidates the pathophysiological mechanisms through which specific vitamins differentially modulate osteoblastic activity and osteoclastic regulation, summarizing contemporary evidence from the molecular to clinical research levels. While vitamin A exhibits dual effects, other vitamins predominantly show positive impacts on bone homeostasis. Oxidative stress and inflammation are key pathological changes associated with osteoporosis. Vitamins play a protective role by enhancing the expression of antioxidant enzymes, activating antioxidant pathways and inhibiting the secretion of inflammatory cytokines, thereby mitigating these conditions. Serum vitamin concentrations exhibit significant correlations with bone mineral density alterations and osteoporosis progression, providing predictive biomarkers for fracture risk assessment. However, serum vitamin profiles exhibit marked heterogeneity across osteoporosis risk strata, necessitating population‑specific therapeutic protocols. Precision‑adjusted supplementation strategies effectively attenuate pathological bone resorption while preserving physiological remodeling homeostasis. The present review systematically delineates the therapeutic potential of vitamins in osteoporotic management, underscoring the necessity for evidence‑based precision nutrient protocols tailored to at‑risk populations to prevent disease progression.
    Keywords:  inflammation; osteoporosis; oxidative stress; vitamin
    DOI:  https://doi.org/10.3892/ijmm.2025.5550
  7. J Cancer Res Clin Oncol. 2025 May 15. 151(5): 167
    High-dose vitamin C promotes mitochondrial biogenesis in HCT116 colorectal cancer cells by regulating the AMPK/PGC-1α signaling pathway.
    RuiYang Hong, Su Min, Jia Huang, Mou Zou, DongYu Zhou, Yun Liang.
       BACKGROUND: Mitochondrial dysfunction is closely associated with cancer development. Colorectal cancer (CRC) cells often exhibit altered energy metabolism, characterized by increased glycolysis and reduced oxidative phosphorylation. Enhancing mitochondrial biogenesis and function may represent a promising therapeutic approach. High-dose vitamin C has demonstrated anti-tumor properties and the ability to reverse the Warburg effect, but its role in regulating mitochondrial biogenesis and function remains unclear.
    METHODS: We evaluated the altered mitochondrial functional status of HCT116 colorectal cancer cells compared to FHC colorectal epithelial cells, assessed the effects of high-dose vitamin C on mitochondrial biogenesis and function in HCT116 cells, and explored the underlying regulatory mechanisms.
    RESULTS: HCT116 cells exhibited mitochondrial dysfunction compared to FHC cells, including decreased expression of electron transport chain complexes III and IV, reduced TFAM levels, and lower mtDNA content. Vitamin C treatment significantly enhanced mitochondrial biogenesis and function, as reflected by increased AMPK phosphorylation, upregulation of PGC-1α, SOD2, NRF2, TFAM, MT-CYB, and MTCO1, elevated mtDNA content, restored membrane potential, enhanced oxidative phosphorylation, and reduced glycolytic activity. Furthermore, vitamin C markedly suppressed HCT116 cell viability and clonogenic capacity, while these effects were substantially diminished by cotreatment with Compound C.
    CONCLUSION: This study demonstrates that high-dose vitamin C ameliorates mitochondrial dysfunction and promotes mitochondrial biogenesis and function in colorectal cancer cells through activation of the AMPK-PGC-1α signaling pathway, thereby suppressing tumor cell proliferation. These findings suggest that vitamin C may serve as a promising therapeutic agent for targeting mitochondrial metabolism in colorectal cancer.
    Keywords:  AMPK; Colorectal cancer; Mitochondrial biogenesis; PGC-1α; Vitamin C
    DOI:  https://doi.org/10.1007/s00432-025-06211-z
This page is being maintained by Thomas Krichel. It was last updated on 2025‒05‒27 at 0:31.