Evidence map›Paper›PMID 39125325›Full record

ReviewNutrients2024

Molecular Mechanisms of Biotin in Modulating Inflammatory Diseases.

Mika Sakurai-Yageta, Yoichi Suzuki

Abstract readReview
In one paragraph

Review in Nutrients, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Natural Molecules for Brain Health and Resilience.International journal of molecular sciences · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Serum vitamins andFrontiers in immunology · 2026
    Observational
  10. Review
  11. Observational
  12. Article
  13. Article
  14. Pathway and protein channel engineering ofSynthetic and systems biotechnology · 2025
    Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Mika Sakurai-YagetaDepartment of Education and Training, Tohoku Medical Megabank Organization, Tohoku University, Sendai 980-8573, Miyagi, Japan.ORCID 0000-0001-5606-3324
Yoichi SuzukiDepartment of Education and Training, Tohoku Medical Megabank Organization, Tohoku University, Sendai 980-8573, Miyagi, Japan.

Funding

Japan Society for the Promotion of Science 23K10909
6 · The paper itself

Abstract

Biotin, also known as vitamin B7 or vitamin H, is a water-soluble B-complex vitamin and serves as an essential co-enzyme for five specific carboxylases. Holocarboxylase synthase (HCS) activates biotin and facilitates its covalent attachment to these enzymes, while biotinidase releases free biotin in the biotin cycle. The transport of biotin, primarily from the intestine, is mediated by the sodium-dependent multi-vitamin transporter (SMVT). Severe biotin deficiency leads to multiple carboxylase deficiency. Moreover, biotin is crucial to glucose and lipid utilization in cellular energy production because it modulates the expression of metabolic enzymes via various signaling pathways and transcription factors. Biotin also modulates the production of proinflammatory cytokines in the immune system through similar molecular mechanisms. These regulatory roles in metabolic and immune homeostasis connect biotin to conditions such as diabetes, dermatologic manifestations, and multiple sclerosis. Furthermore, deficiencies in biotin and SMVT are implicated in inflammatory bowel disease, affecting intestinal inflammation, permeability, and flora. Notably, HCS and probably biotin directly influence gene expression through histone modification. In this review, we summarize the current knowledge on the molecular aspects of biotin and associated molecules in diseases related to both acute inflammatory responses and chronic inflammation, and discuss the potential therapeutic applications of biotin.

Indexed as

BiotinInflammationAnimalsBiotinidase DeficiencyCytokinesHumansInflammatory Bowel DiseasesBiotinCytokinesbiotinbiotinidasediabetesholocarboxylase synthaseinflammatory bowel diseaseproinflammatory cytokineSMVT

Identifiers

PMID39125325
PMCPMC11314543

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.