Evidence map›Paper›PMID 31489936›Full record

ArticleNutrients2019

Dietary Fat-Accelerating Leptin Signaling Promotes Protumorigenic Gastric Environment in Mice.

Seiya Arita, Takumi Ogawa, Yuta Murakami, Yuta Kinoshita, Masaharu Okazaki, Kyoko Inagaki-Ohara

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2019. 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
1.0field-weighted citation impact, top 26% 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, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Microbiota and gastric cancer: from molecular mechanisms to therapeutic strategies.Frontiers in cellular and infection microbiology · 2025
    Review
  5. The influence ofComputational and structural biotechnology journal · 2024
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. A Variant ofPharmacogenomics and personalized medicine · 2020
    Article
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 at 1 institution in 1 country.

Seiya AritaDivision of Host Defense, Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, 5562 Nanatsuka, Shobara, Hiroshima 727-0023, Japan.
Takumi OgawaDivision of Host Defense, Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, 5562 Nanatsuka, Shobara, Hiroshima 727-0023, Japan.
Yuta MurakamiDivision of Host Defense, Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, 5562 Nanatsuka, Shobara, Hiroshima 727-0023, Japan.
Yuta KinoshitaDivision of Host Defense, Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, 5562 Nanatsuka, Shobara, Hiroshima 727-0023, Japan.
Masaharu OkazakiDivision of Host Defense, Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, 5562 Nanatsuka, Shobara, Hiroshima 727-0023, Japan.
Kyoko Inagaki-OharaDivision of Host Defense, Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, 5562 Nanatsuka, Shobara, Hiroshima 727-0023, Japan. k-inagaki@pu-hiroshima.ac.jp.
Prefectural University of Hiroshima · JP

Funding

Prefectural University of Hiroshima Research Grant Program (A) 2
6 · The paper itself

Abstract

Excess of fat intake leads to obesity and causes a variety of metabolic diseases and cancer. We previously demonstrated that high-lard diet induces intestinal metaplasia, a precancerous lesion of the stomach mediated by leptin signaling. This study aims to investigate which kinds of dietary fat cause the intestinal metaplasia onset. We fed eight kinds of high-fat diets (HFDs) of animal or plant origin to mice evaluated their effect on gastric pathogenesis. Five types of dietary fat were divided according to their observed effects: Obese with high metaplasia (group I; beef tallow, lard, and hydrogenated coconut oil), non-obese with high metaplasia (group II; linseed oil), obese without metaplasia (group III; corn oil and olive oil), non-obese without metaplasia (group IV, soybean oil) and lean without metaplasia (group V; cocoa butter). The group I and II diets induced leptin, phosphorylated leptin receptor (ObR), signal transducer and activator 3 (STAT3), and increased intracellular β-catenin accumulation in the stomach. Moreover, mice fed these HFDs with 1-methyl-3-nitro-1-nitrosoguanidine (MNNG), a gastric carcinogen, and further accelerated dysplasia in the stomach.

Indexed as

Animalsbeta CateninCarcinogenesisDietary FatsDiet, High-FatDisease Models, AnimalGastric MucosaLeptinMetaplasiaMiceObesityReceptors, LeptinSignal TransductionSTAT3 Transcription FactorStomachbeta CateninCTNNB1 protein, mouseDietary FatsLeptinReceptors, LeptinStat3 protein, mouseSTAT3 Transcription Factorhigh-fatleptinmicrobiotaprotumorigenesisstomach

Identifiers

PMID31489936
PMCPMC6770546
OpenAlexW2971548620

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.