Evidence map›Paper›PMID 29976400›Full record

ArticleJournal of food and drug analysis2018

Tetrahydrocurcumin ameliorates free fatty acid-induced hepatic steatosis and improves insulin resistance in HepG2 cells.

Jin-Wun Chen, Zwe-Ling Kong, Mei-Ling Tsai, Chih-Yu Lo, Chi-Tang Ho, Ching-Shu Lai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of food and drug analysis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

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  6. The Hypoglycemic Activity ofGels (Basel, Switzerland) · 2025
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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

6 authors.

Jin-Wun ChenDepartment of Seafood Science, National Kaohsiung Marine University, Kaohsiung, 811, Taiwan, ROC.
Zwe-Ling KongDepartment of Food Science, National Taiwan Ocean University, Keelung, 202, Taiwan, ROC.
Mei-Ling TsaiDepartment of Seafood Science, National Kaohsiung Marine University, Kaohsiung, 811, Taiwan, ROC.
Chih-Yu LoDepartment of Food Science, National Chiayi University, Chiayi, 600, Taiwan, ROC.
Chi-Tang HoDepartment of Food Science, Rutgers University, New Brunswick, NJ, 08901, USA.
Ching-Shu LaiDepartment of Seafood Science, National Kaohsiung Marine University, Kaohsiung, 811, Taiwan, ROC.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated levels of free fatty acids (FFAs) in the liver, resulting from either increased lipolysis or imbalanced FFAs flux, is a key pathogenic factor of hepatic steatosis. This study was conducted to examine the therapeutic effect of tetrahydrocurcumin (THC), a naturally occurring curcuminoid and a metabolite of curcumin, on oleic acid (OA)-induced steatosis in human hepatocellular carcinoma cells and to elucidate the underlying mechanism. HepG2 cells were incubated with OA to induce steatosis, and then treated with various concentrations of THC. The results showed that THC treatment significantly decreased lipid accumulation in OA-treated HepG2 cells, possibly, by inhibiting the expression of the lipogenic proteins, sterol regulatory element-binding protein 1 (SREBP-1c), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid synthase (FAS), and fatty acid-binding protein 4 (FABP4). Moreover, THC attenuated OA-induced hepatic lipogenesis in an adenosine monophosphate-activated protein kinase (AMPK)-dependent manner, which was reversed by pretreatment with an AMPK inhibitor. THC promoted lipolysis and upregulated the expression of genes involved in β-oxidation. Glucose uptake and insulin signaling impaired in HepG2 cells incubated with OA were abated by THC treatment, including phosphorylation of the insulin receptor substrate 1 (IRS-1)/phosphoinositide 3-kinase (PI3K)/Akt and downstream signaling pathways, forkhead box protein O1 (FOXO1) and glycogen synthase kinase 3 β (GSK3β), which are involved in gluconeogenesis and glycogen synthesis, respectively. Altogether, these results demonstrated the novel therapeutic benefit of THC against hepatic steatosis and, consequently, a potential treatment for non-alcoholic fatty liver disease (NAFLD).

Indexed as

Insulin ResistanceCurcuminFatty Acid-Binding ProteinsFatty Acids, NonesterifiedFatty LiverGlucoseHep G2 CellsHumansLipogenesisOleic AcidPPAR alphaSterol Regulatory Element Binding Protein 1CurcuminFABP4 protein, humanFatty Acid-Binding ProteinsFatty Acids, NonesterifiedGlucoseOleic AcidPPAR alphaSterol Regulatory Element Binding Protein 1tetrahydrocurcuminAMPKHepG2Insulin resistanceSteatosisTetrahydrocurcumin

Identifiers

PMID29976400
PMCPMC9303024

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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.