Evidence map›Paper›PMID 29391540›Full record

ArticleExperimental & molecular medicine2018

4-hydroxy-3-methoxycinnamic acid regulates orexigenic peptides and hepatic glucose homeostasis through phosphorylation of FoxO1.

Ann W Kinyua, Chang Mann Ko, Khanh V Doan, Dong Joo Yang, My Khanh Q Huynh, Sang Hyun Moh, Yun-Hee Choi, Ki Woo Kim

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  11. Mulberry Bark Alleviates Effect of STZ Inducing Diabetic Mice through Negatively Regulating FoxO1.Evidence-based complementary and alternative medicine : eCAM · 2019
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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

8 authors at 1 institution in 1 country.

Ann W KinyuaDepartments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea.
Chang Mann KoDepartments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea.
Khanh V DoanDepartments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea.
Dong Joo YangDepartments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea.
My Khanh Q HuynhDepartments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea.
Sang Hyun MohAnti-aging Research Institute of BIO-FD&C Co. Ltd., Incheon, Republic of Korea.
Yun-Hee ChoiAnti-aging Research Institute of BIO-FD&C Co. Ltd., Incheon, Republic of Korea.
Ki Woo KimDepartments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea.
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

4-hydroxy-3-methoxycinnamic acid (ferulic acid, FA) is known to have numerous beneficial health effects, including anti-obesity and anti-hyperglycemic properties. However, the molecular networks that modulate the beneficial FA-induced metabolic effects have not been well elucidated. In this study, we explored the molecular mechanisms mediating the beneficial metabolic effects of FA. In mice, FA protected against high-fat diet-induced weight gain, reduced food intake and exhibited an overall improved metabolic phenotype. The food intake suppression by FA was accompanied by a specific reduction in hypothalamic orexigenic neuropeptides, including agouti-related protein and neuropeptide Y, with no significant changes in the anorexigenic peptides pro-opiomelanocortin and cocaine and amphetamine-regulated transcript. FA treatment also inhibited fat accumulation in the liver and white adipose tissue and suppressed the expression of gluconeogenic genes, including phosphoenolpyruvate carboxylase and glucose-6-phosphatase. Furthermore, we show that FA phosphorylated and inactivated the transcription factor FoxO1, which positively regulates the expression of gluconeogenic and orexigenic genes, providing evidence that FA might exert its beneficial metabolic effects through inhibition of FoxO1 function in the periphery and the hypothalamus.

Indexed as

AnimalsBiomarkersCell LineCoumaric AcidsDiet, High-FatEnergy MetabolismForkhead Box Protein O1Gene Expression RegulationGlucoseHomeostasisHypothalamusLiverMaleMiceNeuropeptidesPhosphorylationBiomarkersCoumaric Acidsferulic acidForkhead Box Protein O1GlucoseNeuropeptides

Identifiers

PMID29391540
PMCPMC5903816
OpenAlexW2787696203

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.