Evidence map›Paper›PMID 35461903›Full record

ArticleThe Journal of nutritional biochemistry2022

Sulforaphane induces lipophagy through the activation of AMPK-mTOR-ULK1 pathway signaling in adipocytes.

Masashi Masuda, Risa Yoshida-Shimizu, Yuki Mori, Kohta Ohnishi, Yuichiro Adachi, Maiko Sakai, Serina Kabutoya, Hirokazu Ohminami, Hisami Yamanaka-Okumura, Hironori Yamamoto and 2 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Lipophagy and lipid droplets in neurodegeneration.Trends in pharmacological sciences · 2026
    Review
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  18. Erucin, a Natural Isothiocyanate, Prevents Polyglutamine-Induced Toxicity inInternational journal of molecular sciences · 2024
    Article
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  20. 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

12 authors at 3 institutions in 2 countries.

Masashi MasudaDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan. Electronic address: masuda.masashi@tokushima-u.ac.jp.
Risa Yoshida-ShimizuDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Yuki MoriDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Kohta OhnishiDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Yuichiro AdachiDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Maiko SakaiDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Serina KabutoyaDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Hirokazu OhminamiDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Hisami Yamanaka-OkumuraDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Hironori YamamotoDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan; Department of Health and Nutrition, Faculty of Human Life, Jin-ai University, Echizen, Fukui, Japan; Department of Nephrology, Faculty of Medical Sciences, University of Fukui, Fukui, Japan.
Makoto MiyazakiDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
Yutaka TaketaniDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushma, Tokushima, Japan.
Tokushima University · JPUniversity of Colorado Denver · USUniversity of Fukui · JP

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Edward L Melanson · 1995 to 2026
$32.6M
The role of MLKL in the regulation of vascular calcification in CKDR01HL132318 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MIYAZAKI, MAKOTO · 2016 to 2025
$3.8M
A Novel Driver of Hyperphosphatemia and Vascular Calcification in CKDR01DK124901 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI BLAINE, JUDITH T.,, MIYAZAKI, MAKOTO · 2021 to 2024
$1.9M
The contributory role of microbial metabolite in the pathogenesis of CKD-dependent vascular calcificationR01HL133545 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MIYAZAKI, MAKOTO · 2018 to 2021
$1.9M
NHLBI NIH HHS R01 HL132318NHLBI NIH HHS R01 HL133545NIDDK NIH HHS P30 DK048520NIDDK NIH HHS R01 DK124901
6 · The paper itself

Abstract

Lipophagy, a form of selective autophagy, degrades lipid droplet (LD) in adipose tissue and the liver. The chemotherapeutic isothiocyanate sulforaphane (SFN) contributes to lipolysis through the activation of hormone-sensitive lipase and the browning of white adipocytes. However, the details concerning the regulation of lipolysis in adipocytes by SFN-mediated autophagy remain unclear. In this study, we investigated the effects of SFN on autophagy in the epididymal fat of mice fed a high-fat diet (HFD) or control-fat diet and on the molecular mechanisms of autophagy in differentiated 3T3-L1 cells. Western blotting revealed that the protein expression of lipidated LC3 (LC3-II), an autophagic substrate, was induced after 3T3-L1 adipocytes treatment with SFN. In addition, SFN increased the LC3-II protein expression in the epididymal fat of mice fed an HFD. Immunofluorescence showed that the SFN-induced LC3 expression was co-localized with LDs in 3T3-L1 adipocytes and with perilipin, the most abundant adipocyte-specific protein, in adipocytes of mice fed an HFD. Next, we confirmed that SFN activates autophagy flux in differentiated 3T3-L1 cells using the mCherry-EGFP-LC3 and GFP-LC3-RFP-LC3ΔG probe. Furthermore, we examined the induction mechanisms of autophagy by SFN in 3T3-L1 adipocytes using western blotting. ATG5 knockdown partially blocked the SFN-induced release of fatty acids from LDs in mature 3T3-L1 adipocytes. SFN time-dependently elicited the phosphorylation of AMPK, the dephosphorylation of mTOR, and the phosphorylation of ULK1 in differentiated 3T3-L1 cells. Taken together, these results suggest that SFN may provoke lipophagy through AMPK-mTOR-ULK1 pathway signaling, resulting in partial lipolysis of adipocytes.

Indexed as

AMP-Activated Protein KinasesAutophagy-Related Protein-1 HomologIsothiocyanatesTOR Serine-Threonine Kinases3T3-L1 CellsAdipocytes, WhiteAnimalsAutophagyLipolysisMiceSignal TransductionSulfoxidesAMP-Activated Protein KinasesAutophagy-Related Protein-1 HomologIsothiocyanatesmTOR protein, mousesulforaphaneSulfoxidesTOR Serine-Threonine KinasesUlk1 protein, mouseAdiposeAutophagyCell biologyDietary factorsLipid dropletsObesity

Identifiers

PMID35461903
PMCPMC9447841
OpenAlexW4224218716

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.