Evidence map›Paper›PMID 24978197›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2014

Endogenous ω-3 polyunsaturated fatty acid production confers resistance to obesity, dyslipidemia, and diabetes in mice.

Jie Li, Fanghong R Li, Dong Wei, Wei Jia, Jing X Kang, Maja Stefanovic-Racic, Yifan Dai, Allan Z Zhao

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 60 citations in OpenAlex.

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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 5 institutions in 2 countries.

Jie LiDepartment of Cell Biology and Physiology (J.L.) and Division of Endocrinology and Metabolism (M.S.-R.), University of Pittsburgh, Pittsburgh, Pennsylvania 15261; Department of Pathology (F.R.L), The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China; Department of Endocrinology (D.W.), The Second People's Hospital of Chengdu, Chengdu 610017, China; Surgery (W.J.), West China Hospital, Sichuan University, Chengdu 610041, China; Department of Medicine (J.X.K.), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114; and State Key Laboratory of Reproductive Medicine (F.R.L., Y.D., A.Z.Z.), The Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Fanghong R Li
Dong Wei
Wei Jia
Jing X Kang
Maja Stefanovic-Racic
Yifan Dai
Allan Z Zhao
Nanjing Medical University · CNUniversity of Pittsburgh · USChengdu Second People's Hospital · CNMassachusetts General Hospital · USWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the well-documented health benefits of ω-3 polyunsaturated fatty acids (PUFAs), their use in clinical management of hyperglycemia and obesity has shown little success. To better define the mechanisms of ω-3 PUFAs in regulating energy balance and insulin sensitivity, we deployed a transgenic mouse model capable of endogenously producing ω-3 PUFAs while reducing ω-6 PUFAs owing to the expression of a Caenorhabditis elegans fat-1 gene encoding an ω-3 fatty acid desaturase. When challenged with high-fat diets, fat-1 mice strongly resisted obesity, diabetes, hypercholesterolemia, and hepatic steatosis. Endogenous elevation of ω-3 PUFAs and reduction of ω-6 PUFAs did not alter the amount of food intake but led to increased energy expenditure in the fat-1 mice. The requirements for the levels of ω-3 PUFAs as well as the ω-6/ω-3 ratios in controlling blood glucose and obesity are much more stringent than those in lipid metabolism. These metabolic phenotypes were accompanied by attenuation of the inflammatory state because tissue levels of prostaglandin E2, leukotriene B4, monocyte chemoattractant protein-1, and TNF-α were significantly decreased. TNF-α-induced nuclear factor-κB signaling was almost completely abolished. Consistent with the reduction in chronic inflammation and a significant increase in peroxisome proliferator-activated receptor-γ activity in the fat-1 liver tissue, hepatic insulin signaling was sharply elevated. The activities of prolipogenic regulators, such as liver X receptor, stearoyl-CoA desaturase-1, and sterol regulatory element binding protein-1 were sharply decreased, whereas the activity of peroxisome proliferator-activated receptor-α, a nuclear receptor that facilitates lipid β-oxidation, was markedly increased. Thus, endogenous conversion of ω-6 to ω-3 PUFAs via fat-1 strongly protects against obesity, diabetes, inflammation, and dyslipidemia and may represent a novel therapeutic modality to treat these prevalent disorders.

Indexed as

AdiposityAnimalsCadherinsDiabetes Mellitus, ExperimentalDiet, High-FatDisease ResistanceDyslipidemiasFatty Acids, Omega-3Gene ExpressionInflammationLipogenesisLiverMaleMice, Inbred C57BLMice, TransgenicObesityCadherinsfat1 protein, mouseFatty Acids, Omega-3

Identifiers

PMID24978197
PMCPMC5414802
OpenAlexW2013333442

What OpenQuestion holds

Textmetadata
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.