Evidence map›Paper›PMID 30987128›Full record

ArticleInternational journal of molecular sciences2019

Capsaicin Targets Lipogenesis in HepG2 Cells Through AMPK Activation, AKT Inhibition and PPARs Regulation.

Alicia Bort, Belén G Sánchez, Pedro A Mateos-Gómez, Inés Díaz-Laviada, Nieves Rodríguez-Henche

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Modulation of Hepatic Cholesterol-Related Pathways byMolecules (Basel, Switzerland) · 2026
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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

5 authors at 1 institution in 1 country.

Alicia BortDepartment of Systems Biology, School of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, E-28871 Madrid, Spain. aliciabort@gmail.com.
Belén G SánchezDepartment of Systems Biology, School of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, E-28871 Madrid, Spain. belensg.88@gmail.com.
Pedro A Mateos-GómezDepartment of Systems Biology, School of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, E-28871 Madrid, Spain. pedroantonio.mateos@uah.es.
Inés Díaz-LaviadaDepartment of Systems Biology, School of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, E-28871 Madrid, Spain. ines.diazlaviada@uah.es.
Nieves Rodríguez-HencheDepartment of Systems Biology, School of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, E-28871 Madrid, Spain. nieves.rhenche@uah.es.
Universidad de Alcalá · ES

Funding

FUNDACIÓN TATIANA PÉREZ DE GUZMÁN Patrocinio 2013-001 and Patrocinio 2019-001
6 · The paper itself

Abstract

Obesity, a major risk factor for chronic diseases such as type 2 diabetes (T2D), represents a serious primary health problem worldwide. Dietary habits are of special interest to prevent and counteract the obesity and its associated metabolic disorders, including lipid steatosis. Capsaicin, a pungent compound of chili peppers, has been found to ameliorate diet-induced obesity in rodents and humans. The purpose of this study was to examine the effect of capsaicin on hepatic lipogenesis and to delineate the underlying signaling pathways involved, using HepG2 cells as an experimental model. Cellular neutral lipids, stained with BODIPY493/503, were quantified by flow cytometry, and the protein expression and activity were determined by immunoblotting. Capsaicin reduced basal neutral lipid content in HepG2 cells, as well that induced by troglitazone or by oleic acid. This effect of capsaicin was prevented by dorsomorphin and GW9662, pharmacological inhibitors of AMPK and PPARγ, respectively. In addition, capsaicin activated AMPK and inhibited the AKT/mTOR pathway, major regulators of hepatic lipogenesis. Furthermore, capsaicin blocked autophagy and increased PGC-1α protein. These results suggest that capsaicin behaves as an anti-lipogenic compound in HepG2 cells.

Indexed as

AMP-Activated Protein KinasesAutophagyCapsaicinEnzyme ActivationHep G2 CellsHumansLipidsLipogenesisModels, BiologicalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPeroxisome Proliferator-Activated ReceptorsProto-Oncogene Proteins c-aktUp-RegulationAMP-Activated Protein KinasesCapsaicinLipidsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPeroxisome Proliferator-Activated ReceptorsProto-Oncogene Proteins c-aktAKTAMPKcapsaicinHepG2lipid metabolismPPARαPPARγ

Identifiers

PMID30987128
PMCPMC6480012
OpenAlexW2933365160

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.