Evidence map›Paper›PMID 26839577›Full record

ArticleNutrition & metabolism2016

Leptin receptor signaling is required for high-fat diet-induced atrophic gastritis in mice.

Kyoko Inagaki-Ohara, Shiki Okamoto, Kazuyo Takagi, Kumiko Saito, Seiya Arita, Lijun Tang, Tetsuji Hori, Hiroaki Kataoka, Satoshi Matsumoto, Yasuhiko Minokoshi

Open access · goldAbstract read
In one paragraph

Article in Nutrition & metabolism, 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
3.5field-weighted citation impact, top 8% 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, 24 citations in OpenAlex.

  1. Article
  2. Diet-Induced Obesity ExacerbatesbioRxiv : the preprint server for biology · 2026
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  10. Role of Leptin in the Digestive System.Frontiers in pharmacology · 2021
    Review
  11. Review
  12. Review
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  14. Article
  15. Gastric Leptin and Tumorigenesis: Beyond Obesity.International journal of molecular sciences · 2019
    Review
  16. Article
  17. 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

10 authors at 5 institutions in 1 country.

Kyoko Inagaki-OharaResearch Institute, National Center for Global Health and Medicine (NCGM), 1-21-1, Toyama Shinjuku, Tokyo, 162-0052 Japan ; Division of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences (NIPS), 38 Nishigonaka Myodaiji, Okazaki, Aichi 444-8585 Japan ; Division of Host Defense, Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, 562 Nanatsuka, Shobara, Hiroshima 727-0023 Japan.
Shiki OkamotoDivision of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences (NIPS), 38 Nishigonaka Myodaiji, Okazaki, Aichi 444-8585 Japan.
Kazuyo TakagiDivision of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences (NIPS), 38 Nishigonaka Myodaiji, Okazaki, Aichi 444-8585 Japan.
Kumiko SaitoDivision of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences (NIPS), 38 Nishigonaka Myodaiji, Okazaki, Aichi 444-8585 Japan.
Seiya AritaDivision of Host Defense, Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, 562 Nanatsuka, Shobara, Hiroshima 727-0023 Japan.
Lijun TangDivision of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences (NIPS), 38 Nishigonaka Myodaiji, Okazaki, Aichi 444-8585 Japan.
Tetsuji HoriYakult Central Institute for Microbiological Research, 5-11 Izumi, Kunitachi, Tokyo, 186-8650 Japan.
Hiroaki KataokaSection of Oncopathology and Regenerative Biology, Department of Pathology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692 Japan.
Satoshi MatsumotoYakult Central Institute for Microbiological Research, 5-11 Izumi, Kunitachi, Tokyo, 186-8650 Japan.
Yasuhiko MinokoshiDivision of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences (NIPS), 38 Nishigonaka Myodaiji, Okazaki, Aichi 444-8585 Japan.
National Institute for Physiological Sciences · JPYakult Central Institute · JPNational Center for Global Health and Medicine · JPPrefectural University of Hiroshima · JPUniversity of Miyazaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity increases the risk for malignancies in various tissues including the stomach. Atrophic gastritis with precancerous lesions is an obesity-associated disease; however, the mechanisms that underlie the development of obesity-associated atrophic gastritis are unknown. Leptin is a hormone derived from stomach as well as adipose tissue and gastric leptin is involved in the development of gastric cancer. The aim of the current study is to investigate the involvement of leptin receptor signaling in the development of atrophic gastritis during diet-induced obesity.

methodsMale C57BL/6, ob/ob and db/db mice were fed a high-fat diet (HFD) or a control diet (CD) from 1 week to 5 months. Pathological changes of the gastric mucosa and the expression of molecules associated with atrophic gastritis were evaluated in these mice.

resultsHFD feeding induced gastric mucosal hyperplasia with increased gastric leptin expression. Mucosal hyperplasia was accompanied by a higher frequency of Ki67-positive proliferating cells and atrophy of the gastric glands in the presence of inflammation, which increased following HFD feeding. Activation of ObR signaling-associated molecules such as ObR, STAT3, Akt, and ERK was detected in the gastric mucosa of mice fed the HFD for 1 week. The morphological alterations associated with gastric mucosal atrophy and the expression of Muc2 and Cdx2 resemble those associated with human intestinal metaplasia. In contrast to wild-type mice, leptin-deficient ob/ob mice and leptin receptor-mutated db/db mice did not show increased Cdx2 expression in response to HFD feeding.

conclusionTogether, these results suggest that activation of the leptin signaling pathway in the stomach is required to develop obesity-associated atrophic gastritis.

Indexed as

Atrophic gastritisHigh-fat dietLeptinObesity

Identifiers

PMID26839577
PMCPMC4736478
OpenAlexW2259102595

What OpenQuestion holds

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LicenceCC BY
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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.