Evidence map›Paper›PMID 30283077›Full record

ArticleInternational journal of obesity (2005)2019

Ascorbic acid inhibits visceral obesity and nonalcoholic fatty liver disease by activating peroxisome proliferator-activated receptor α in high-fat-diet-fed C57BL/6J mice.

Hyunghee Lee, Jiwon Ahn, Soon Shik Shin, Michung Yoon

Abstract read
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In one paragraph

Article in International journal of obesity (2005), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
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

36 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Effects ofNutrients · 2022
    Trial
  3. Review
  4. Frontiers in immunology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Frontiers in microbiology · 2025
    Article
  9. Pummelo fruit extract (Toxicology research · 2024
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Association Between Serum Vitamin C and Non-alcoholic Fatty Liver Disease: A Cross-sectional Study.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    Article
  18. Article
  19. Review
  20. Review
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

4 authors at 3 institutions in 1 country.

Hyunghee Lee *Department of Biomedical Engineering, Mokwon University, Daejeon, 35349, South Korea.
Jiwon Ahn *Genome Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, South Korea.
Soon Shik ShinDepartment of Formula Sciences, College of Korean Medicine, Dongeui University, Busan, 47340, Korea. ssshin@deu.ac.kr.
Michung YoonDepartment of Biomedical Engineering, Mokwon University, Daejeon, 35349, South Korea. yoon60@mokwon.ac.kr.
Mokwon University · KRDong-Eui University · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesAscorbic acid is a known cofactor in the biosynthesis of carnitine, a molecule that has an obligatory role in fatty acid oxidation. Our previous studies have demonstrated that obesity is regulated effectively through peroxisome proliferator-activated receptor α (PPARα)-mediated fatty acid β-oxidation. Thus, this study aimed to determine whether ascorbic acid can inhibit obesity and nonalcoholic fatty liver disease (NAFLD) in part through the actions of PPARα.

designAfter C57BL/6J mice received a low-fat diet (LFD, 10% kcal fat), a high-fat diet (HFD, 45% kcal fat), or the same HFD supplemented with ascorbic acid (1% w/w) (HFD-AA) for 15 weeks, variables and determinants of visceral obesity and NAFLD were examined using metabolic measurements, histology, and gene expression.

resultsCompared to HFD-fed obese mice, administration of HFD-AA to obese mice reduced body weight gain, visceral adipose tissue mass, and visceral adipocyte size without affecting food consumption profiles. Concomitantly, circulating ascorbic acid concentrations were significantly higher in HFD-AA mice than in HFD mice. Ascorbic acid supplementation increased the mRNA levels of PPARα and its target enzymes involved in fatty acid β-oxidation in visceral adipose tissues. Consistent with the effects of ascorbic acid on visceral obesity, ascorbic acid not only inhibited hepatic steatosis but also increased the mRNA levels of PPARα-dependent fatty acid β-oxidation genes in livers. Similarly, hepatic inflammation, fibrosis, and apoptosis were also decreased during ascorbic acid-induced inhibition of visceral obesity. In addition, serum levels of alanine aminotransferase, aspartate aminotransferase, total cholesterol, and LDL cholesterol were lower in HFD-AA-fed mice than in those of HFD-fed mice.

conclusionsThese results suggest that ascorbic acid seems to suppress HFD-induced visceral obesity and NAFLD in part through the activation of PPARα.

Indexed as

Diet, High-FatAnimalsAscorbic AcidDietary SupplementsDiet, Fat-RestrictedFatty AcidsGene ExpressionIntra-Abdominal FatLiverMaleMiceMice, Inbred C57BLMice, ObeseNon-alcoholic Fatty Liver DiseaseObesity, AbdominalOxidation-ReductionAscorbic AcidFatty AcidsPPAR alpha

Identifiers

PMID30283077
OpenAlexW2895085109

What OpenQuestion holds

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Registered trials

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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.