Evidence map›Paper›PMID 36771210›Full record

ArticleNutrients2023

L-Fucose Suppresses Lipid Accumulation via the AMPK Pathway in 3T3-L1 Adipocytes.

Tomohiko Nakao, Shiro Otaki, Yuri Kominami, Soichi Watanabe, Miho Ito, Teruki Aizawa, Yusuke Akahori, Hideki Ushio

Abstract read
In one paragraph

Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. The antihyperglycemic potential ofFood science and biotechnology · 2025
    Article
  3. Article
  4. Metabolomics: Uncovering Insights into Obesity and Diabetes.International journal of molecular sciences · 2025
    Article
  5. Article
  6. 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

8 authors.

Tomohiko NakaoDepartment of Aquatic Bioscience, Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo 113-8657, Japan.
Shiro OtakiDepartment of Aquatic Bioscience, Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo 113-8657, Japan.
Yuri KominamiDepartment of Aquatic Bioscience, Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo 113-8657, Japan.
Soichi WatanabeDepartment of Aquatic Bioscience, Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo 113-8657, Japan.
Miho ItoYaizu Suisankagaku Industry Co., Ltd., 5-8-13 Kogawa-shimmachi, Yaizu, Shizuoka 425-8570, Japan.
Teruki AizawaYaizu Suisankagaku Industry Co., Ltd., 5-8-13 Kogawa-shimmachi, Yaizu, Shizuoka 425-8570, Japan.
Yusuke AkahoriYaizu Suisankagaku Industry Co., Ltd., 5-8-13 Kogawa-shimmachi, Yaizu, Shizuoka 425-8570, Japan.
Hideki UshioDepartment of Aquatic Bioscience, Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo 113-8657, Japan.

Funding

Japan Science and Technology Agency JPMJTR194EJapan Society for the Promotion of Science 19H00947
6 · The paper itself

Abstract

L-fucose (Fuc), a monosaccharide with different biological functions in various organisms, exhibits potent anti-obesity effects in obese mice. However, the mechanisms underlying its anti-obesity effects remain largely unknown. In this study, we aimed to investigate the effects of Fuc on lipid metabolism and insulin signaling in 3T3-L1 adipocytes. We found that Fuc treatment suppressed lipid accumulation during adipocyte differentiation. Additionally, Fuc treatment enhanced the phosphorylation of AMP-activated kinase (AMPK) and its downstream pathways, responsible for the regulation of fatty acid oxidation and lipolysis. Furthermore, Fuc-induced activation of the AMPK pathway was diminished by the AMPK inhibitor Compound C, and Fuc treatment considerably promoted glucose uptake via Akt activation in an insulin-resistant state. These findings provide a basis for elucidating the mechanism underlying the anti-obesity effect of Fuc, which may, in the future, be considered as a therapeutic compound for treating obesity and related diseases.

Indexed as

AMP-Activated Protein KinasesFucose3T3-L1 CellsAdipocytesAdipogenesisAnimalsInsulinLipidsMiceObesityAMP-Activated Protein KinasesFucoseInsulinLipidsAMPKanti-obesityinsulin signalingL-fucoselipolysis

Identifiers

PMID36771210
PMCPMC9919779

What OpenQuestion holds

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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.