Evidence map›Paper›PMID 28469249›Full record

ArticleScientific reports2017

Protectin DX ameliorates palmitate- or high-fat diet-induced insulin resistance and inflammation through an AMPK-PPARα-dependent pathway in mice.

Tae Woo Jung, Hyoung-Chun Kim, A M Abd El-Aty, Ji Hoon Jeong

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. Modeling human heterogeneity of obesity with diversity outbred mice reveals a fat mass-dependent therapeutic window for resolvin E1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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  17. Echocardiographic Changes in Newly Diagnosed Type 2 Diabetes Mellitus Patients with and without Hypertension.Medical science monitor : international medical journal of experimental and clinical research · 2020
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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

4 authors.

Tae Woo JungResearch Administration Team, Seoul National University Bundang Hospital, Gyeonggi, Republic of Korea.
Hyoung-Chun KimNeuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, Republic of Korea.
A M Abd El-AtyDepartment of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, Konkuk University, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0001-6596-7907
Ji Hoon JeongDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea. jhjeong3@cau.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protectin DX (PDX), a double lipoxygenase derivative of docosahexaenoic acid, has been reported to attenuate inflammation and insulin resistance. In the current study, we explored the effects of PDX on hyperlipidemia-induced insulin resistance and inflammation through AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor α (PPARα). PDX attenuated the impairment of insulin receptor substrate 1/Akt-mediated insulin signaling in palmitate-treated differentiated C2C12 cells and soleus skeletal muscle of HFD-fed mice. Furthermore, PDX treatment significantly ameliorated HFD-induced weight gain and improved glucose tolerance in mice. Nuclear factor kB nuclear translocation, inhibitory kBα phosphorylation, and expression of proinflammatory cytokines were markedly attenuated by PDX in both in vitro and in vivo models. PDX treatment markedly augmented AMPK phosphorylation and PPARα expression in C2C12 cells and in skeletal muscle of mice. AMPK- and PPARα-specific siRNAs significantly abrogated the suppressive effects of PDX on palmitate-induced insulin resistance and inflammation. Furthermore, PDX markedly stimulated the expression of genes related to fatty acid oxidation. These effects of PDX were significantly suppressed by AMPK and PPARα siRNAs. In conclusion, our results demonstrate that PDX ameliorates insulin resistance and inflammation and stimulates fatty acid oxidation through AMPK- and PPARα-mediated pathways in skeletal muscle.

Indexed as

Insulin ResistanceAMP-Activated Protein KinasesAnimalsAnti-Inflammatory Agents, Non-SteroidalCells, CulturedDiet, High-FatDocosahexaenoic AcidsHypoglycemic AgentsInflammationMaleMice, Inbred C57BLMuscle, SkeletalPalmitatesPPAR alphaSignal Transduction10,17-dihydroxydocosa-4,7,11,13,15,19-hexaenoic acidAMP-Activated Protein KinasesAnti-Inflammatory Agents, Non-SteroidalDocosahexaenoic AcidsHypoglycemic AgentsPalmitatesPPAR alpha

Identifiers

PMID28469249
PMCPMC5431091

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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.