Evidence map›Paper›PMID 27146467›Full record

ArticleInternational journal of obesity (2005)2016

The metabolic response to a high-fat diet reveals obesity-prone and -resistant phenotypes in mice with distinct mRNA-seq transcriptome profiles.

J-Y Choi, R A McGregor, E-Y Kwon, Y J Kim, Y Han, J H Y Park, K W Lee, S-J Kim, J Kim, J W Yun and 1 more

Abstract read
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In one paragraph

Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

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  13. Impaired lipid metabolism by age-dependent DNA methylation alterations accelerates aging.Proceedings of the National Academy of Sciences of the United States of America · 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

11 authors at 7 institutions in 1 country.

J-Y ChoiDepartment of Food Sciences and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
R A McGregorCardiovascular and Metabolic Disease Center, Inje University, Busan, Republic of Korea.
E-Y KwonDepartment of Food Sciences and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
Y J KimDepartment of Food Sciences and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
Y HanDepartment of Food Sciences and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
J H Y ParkDepartment of Food Sciences and Nutrition, Hallym University, Chuncheon, Republic of Korea.
K W LeeDepartment of Food Science and Technology, Seoul National University, Seoul, Republic of Korea.
S-J KimCHA Cancer Institute, CHA University, Kyunggi-do, Republic of Korea.
J KimCHA Cancer Institute, CHA University, Kyunggi-do, Republic of Korea.
J W YunDepartment of Biotechnology, Daegu University, Kyungsan, Republic of Korea.
M-S ChoiDepartment of Food Sciences and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
Kyungpook National University · KRCHA University · KRDaegu University · KRHallym University · KRInje University · KRKyung Hee University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe aim of this study was to explore the phenotypic differences underpinning obesity susceptibility or resistance based on the metabolic and transcriptional profiling of C57BL/6J mice fed a high-fat diet (HFD).

methodsThe mice were fed either a normal diet or HFD for 12 weeks. After 6 weeks, the mice on HFD were classified as either obesity-prone (OP) or obesity-resistant (OR) depending on the body weight gain.

resultsLipid profiles from plasma and liver significantly improved in OR mice relative to the OP group. Energy expenditure was greater in OR mice than in OP mice, with a simultaneous decrease in body fat mass. Epididymal white adipose tissue (eWAT) and liver were enlarged in OP mice (with visible immune-cell infiltration), but these effects were attenuated in OR mice compared with OP mice. Overall glucose metabolism was enhanced in OR mice compared with OP mice, including homeostasis model assessment for insulin resistance, plasma glucose and insulin concentrations, glucokinase activity and hepatic glycogen. Plasma adipokines and proinflammatory cytokines were upregulated in OP mice, and these changes were attenuated in OR mice. Transcriptomic profiles of eWAT and liver revealed common and divergent patterns of transcriptional changes in OP and OR mice, and pointed to differential metabolic phenotypes of OP and OR mice. There were substantial differences between OP and OR mice in molecular pathways, including atherosclerosis signaling, sperm motility, cAMP-mediated signaling in eWAT; and fibrosis, agranulocyte adhesion and diapedesis, and atherosclerosis signaling in liver.

conclusionsTaken altogether, the results provide robust evidence of major divergence in the transcriptomes, phenotypes and metabolic processes between obesity susceptibility and obesity resistance in the HFD-fed C57BL/6J mice.

Indexed as

Diet, High-FatPhenotypeTranscriptomeAdipose Tissue, WhiteAnimalsCoronary Artery DiseaseDisease Models, AnimalEnergy MetabolismGenetic Predisposition to DiseaseInsulin ResistanceLiverMaleMiceMice, Inbred C57BLObesityRNA, MessengerRNA, Messenger

Identifiers

PMID27146467
OpenAlexW2346359873

What OpenQuestion holds

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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.