bims-vitmet 2025-07-27 papers

Issue of 2025–07–27
five papers selected by
Onurkan Karabulut, Berkeley City College

Metabolites. 2025 Jun 30. pii: 436. [Epub ahead of print]15(7):

Nutri-Epigenetic Regulation of Vitamin D-Impact on Metabolism and Biological Functions: Narrative Review.

Magdalena Kowalówka, Ilona Górna, Marta Karaźniewicz-Łada, Dominika Kusyk, Juliusz Przysławski, Sławomira Drzymała-Czyż.

Vitamin D deficiency is widespread. It increases the risk of several diseases. Therefore, researchers have long studied the factors that influence vitamin D levels in the body. These include its metabolism, catabolism, transport and binding of vitamin D to the receptor VDR. Currently, an increasing number of studies are focusing on genetic factors. Variations in vitamin D levels, including vitamin D deficiency, are under substantial genetic control. There is a reciprocity between the vitamin D system and epigenetic mechanisms. Vitamin D metabolism, on the one hand, is regulated by epigenetic mechanisms and, on the other hand, is involved in regulating epigenetic events. To appraise recent advances in nutrigenomics with its application in public health, several databases, including PubMed, Scopus and Web of Science, were investigated in detail. Nutri-epigenetics deals with the interplay between dietary components and the possible resulting changes in the epigenome. There is, therefore, great potential for the development of nutri-epigenetics. The purpose of the narrative review is to highlight the genetic aspects of vitamin D, its receptor VDR and vitamin D-related gene polymorphisms with a particular focus on vitamin D gene regulation. Particular attention is paid to the vitamin D response index.

Keywords: epigenome; gene expression; nutrigenomics; polymorphism; vitamin D response index

DOI: https://doi.org/10.3390/metabo15070436

Ann Med. 2025 Dec;57(1): 2533429

The role of fat-soluble vitamins on bone metabolism and osteoporosis: a literature review.

Hongyang Li, Wenhai Cao, Lin Tao, Yue Zhu.

PURPOSE: The purpose of this review is to discuss the role of fat-soluble vitamins in bone metabolism and explore whether there is a relationship between each fat-soluble vitamins in the occurrence and development of osteoporosis.
METHODS: We selected several databases, including PubMed, PubMed Central (PMC), Embase, and Web of Science, as the primary sources for the search. Keywords closely related to the subject of this study, such as 'osteoporosis', 'vitamin A', 'vitamin D', 'vitamin E', 'Vitamin K', 'ferroptosis', 'osteoblast' and 'osteoclast', were used in the search. The search deadline is April 20, 2025. All included clinical studies were graded for critical analysis GRADE.
RESULTS: Among 573 reviewed articles, 182 were included (52 met GRADE criteria: A=10, B=26, C=11, D=5; 130 N/A). Vitamins D and K enhance osteoblast differentiation via RUNX2/ALP upregulation. Vitamin A's bone effects remain debated, potentially interacting with vitamin D. Vitamins E and K may jointly regulate bone metabolism as ferroptosis inhibitors.
CONCLUSION: i Fat-soluble vitamins (D, K, E) may positively impact bone mineral density (BMD), while vitamin A's effects remain controversial, potentially harming BMD at high doses. Current single-vitamin studies have limitations; future research should explore combined vitamin interactions to advance osteoporosis diagnosis and treatment.

Keywords: Fat-soluble vitamins; bone; ferroptosis; osteoporosis

DOI: https://doi.org/10.1080/07853890.2025.2533429

Front Nutr. 2025 ;12 1605300

Association between dietary vitamin K intake and lipid metabolism among populations with cardiovascular disease.

Tao Liu, Lili Wang, Qiming Dai, Yesheng Pan.

Background: The objective of this investigation was to examine the correlation between intake of dietary vitamin K and lipid metabolism in cardiovascular disease populations.
Methods: The data for this investigation were obtained from the National Health and Nutrition Examination Survey (NHANES) 2003-2014. The exposure variable was the total daily intake of dietary vitamin K (μg). Triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) comprised the lipid indicators. To investigate the relationship between vitamin K intake and lipid metabolism, the following analyses were conducted: weighted multiple linear regression, smoothing curve fitting, generalized additive models, threshold analysis, subgroup analysis, and sensitivity analyses.
Results: Ultimately, 1,543 participants aged 18 years or older were enrolled. The total daily intake of dietary vitamin K was found to be negatively correlated with TG (β: -15.57, 95% CI: -27.806, -3.333) and TC (β: -6.564, 95% CI: -12.252, -0.877). For each 1 ug increase in the total daily intake of dietary vitamin K, the LDL-C would decrease by 0.510 mg/dl (95% CI: -0.940, -0.078) when the total daily intake of dietary vitamin K was less than 23.7 ug. HDL-C was not influenced by total daily intake of dietary vitamin K. Furthermore, subgroup analyses and sensitivity analyses revealed that an increase in the total daily intake of dietary vitamin K was still negatively associated with TG, TC, and LDL.
Conclusion: The consumption of foods with high vitamin K levels might contribute to the improvement of TC, TG, and LDL-C levels in CVD populations.

Keywords: NHANES; cardiovascular disease; dietary vitamin K; intake; lipid metabolism

DOI: https://doi.org/10.3389/fnut.2025.1605300

J Nutr. 2025 Jul 19. pii: S0022-3166(25)00433-X. [Epub ahead of print]

Dietary fat intake attenuates vitamin A deficiency-associated elastic fiber remodeling and lipid reduction in the alveolar niche in mice.

Lisa-Marie Hoy, Tabea Meier, Natascha Mierswa, Melanie Bornemann, Lea Naasner, Heike Bähre, Natali Froese, Christian Riehle, Christian Mühlfeld, Julia Schipke.

BACKGROUND: Vitamin A deficiency (VAD) and obesity are widespread nutrition-related health conditions that are independently associated with pulmonary remodeling processes linked to lung function decline and respiratory diseases.
OBJECTIVE: This study tested the hypothesis that VAD-related pulmonary alterations are aggravated by diet-induced obesity.
METHODS: 8-week-old C57BL/6J/129Sv mice with a deletion of lecithin-retinol-acyltransferase (Lrat-; impaired vitamin A storage) were fed vitamin A-deficient control diet (CD, n=13) or high-fat diet (HFD, n=15) to induce VAD in lean (CD-VAD, n=13) or obese (HFD-VAD, n=13) animals. Wild-type mice receiving vitamin A-containing CD or HFD served as controls. After 20 weeks, lungs were subjected to structural and molecular analyses by stereology, western blot and HPLC-MS. Statistics used was two-way-ANOVA.
RESULTS: Pulmonary vitamin A reserves were efficiently depleted in CD-VAD and HFD-VAD (p <0.001 compared to controls). In CD-VAD, 76% of pulmonary elastic fibers appeared densely packed (CD: 53%, p <0.01) and expression of fibrillin was 110% higher compared to CD (p <0.01), indicating a higher septal microfibril content. Elastin expression was slightly reduced in HFD- groups (HFD: 14%, HFD-VAD: 16% of respective controls, both p <0.05), whereas neither diet nor VAD affected expression levels of collagen I or III. Lipid droplet volumes decreased by 32% in septal fibroblasts (p <0.05) and by 53% in alveolar epithelial type 2 (AE2) cells in CD-VAD, compared to CD. HFD alone led to a 20% reduction in lung airspace volume, a 13% decrease in septal surface area and a 15% reduction in AE2 cell numbers compared to CD. These VAD- and obesity-related changes were alleviated or absent in HFD-VAD.
CONCLUSION: VAD induced elastic fiber remodeling and lipid droplet reduction in the alveolar region of lean mice, whereas HFD resulted in smaller lungs containing less AE2 cells. Both VAD- and obesity-related effects were attenuated in HFD-VAD, indicating mutually mitigating effects.

Keywords: Lrat-Knockout; Vitamin A deficiency; alveolar epithelial type 2 cells; alveolar region; elastic fiber remodeling; fibrillin-1; lipid depletion; obesity

DOI: https://doi.org/10.1016/j.tjnut.2025.07.010

Epigenomes. 2025 Jul 09. pii: 23. [Epub ahead of print]9(3):

The Fundamental Role of Nutrients for Metabolic Balance and Epigenome Integrity Maintenance.

Ana Paula de Souza, Vitor Marinho, Marcelo Rocha Marques.

Epigenetic modifications act as crucial regulators of gene activity and are influenced by both internal and external environmental factors, with diet being the most impactful external factor. On the other hand, cellular metabolism encompasses a complex network of biochemical reactions essential for maintaining cellular function, and it impacts every cellular process. Many metabolic cofactors are critical for the activity of chromatin-modifying enzymes, influencing methylation and the global acetylation status of the epigenome. For instance, dietary nutrients, particularly those involved in one-carbon metabolism (e.g., folate, vitamins B12 and B6, riboflavin, methionine, choline, and betaine), take part in the generation of S-adenosylmethionine (SAM), which represents the main methyl donor for DNA and histone methylation; α-ketoglutarate and ascorbic acid (vitamin C) act, respectively, as a co-substrate and cofactor for Ten-eleven Translocation (TET), which is responsible for DNA demethylation; and metabolites such as Acetyl-CoA directly impact histone acetylation, linking metabolism of the TCA cycle to epigenetic regulation. Further, bioactive compounds, such as polyphenols, modulate epigenetic patterns by affecting methylation processes or targeting epigenetic enzymes. Since diet and nutrition play a critical role in shaping epigenome functions and supporting human health, this review offers a comprehensive update on recent advancements in metabolism, epigenetics, and nutrition, providing insights into how nutrients contribute to metabolic balance, epigenome integrity maintenance and, consequently, disease prevention.

Keywords: DNA methylation; TCA cycle; diet; epigenetic; histone modification; metabolism; one-carbon cycle

DOI: https://doi.org/10.3390/epigenomes9030023