Evidence map›Paper›PMID 39668067›Full record

ArticleMolecular metabolism2025

Intestinal butyric acid-mediated disruption of gut hormone secretion and lipid metabolism in vasopressin receptor-deficient mice.

Kazuki Harada, Eiji Wada, Yuri Osuga, Kie Shimizu, Reiko Uenoyama, Masami Yokota Hirai, Fumihiko Maekawa, Masao Miyazaki, Yukiko K Hayashi, Kazuaki Nakamura and 1 more

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Article in Molecular metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

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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

2 citing papers in PubMed.

  1. Article
  2. Review
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.

Kazuki HaradaDepartment of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo 153-8902, Japan; Health and Environmental Risk Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan.
Eiji WadaDepartment of Pathophysiology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku, Tokyo 160-8402, Japan.
Yuri OsugaDepartment of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo 153-8902, Japan.
Kie ShimizuDepartment of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan; Division of Life Sciences, Graduate School of Science and Engineering, Saitama University, 255 Shimo-Okubo, Sakura, Saitama 338-8570, Japan.
Reiko UenoyamaThe United Graduate School of Agricultural Sciences, Iwate University, 3-18-8 Ueda, Morioka, Iwate 020-8550, Japan.
Masami Yokota HiraiRIKEN Center for Sustainable Resource Science, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama-city, Kanagawa 230-0045, Japan.
Fumihiko MaekawaHealth and Environmental Risk Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan.
Masao MiyazakiThe United Graduate School of Agricultural Sciences, Iwate University, 3-18-8 Ueda, Morioka, Iwate 020-8550, Japan.
Yukiko K HayashiDepartment of Pathophysiology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku, Tokyo 160-8402, Japan.
Kazuaki NakamuraDepartment of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan; Division of Life Sciences, Graduate School of Science and Engineering, Saitama University, 255 Shimo-Okubo, Sakura, Saitama 338-8570, Japan.
Takashi TsuboiDepartment of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo 153-8902, Japan. Electronic address: takatsuboi@bio.c.u-tokyo.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesArginine vasopressin (AVP), known as an antidiuretic hormone, is also crucial in metabolic homeostasis. Although AVP receptor-deficient mice exhibit various abnormalities in glucose and lipid metabolism, the mechanism underlying these symptoms remains unclear. This study aimed to explore the involvement of the gut hormones including glucagon-like peptide-1 (GLP-1) and microbiota as essential mediators.

methodsWe used the mouse GLP-1-secreting cell line, GLUTag, and performed live cell imaging to examine the contribution of V1a and V1b vasopressin receptors (V1aR and V1bR, respectively) to GLP-1 secretion. We next investigated the hormone dynamics of V1aR-deficient mice (V1aR

resultsAVP induced the increase in intracellular Ca

conclusionsThe deficiency in V1 receptor genes may increase gut butyric acid levels and impair the function of L cells, thus dysregulating lipid homeostasis in the brown adipose tissue and skeletal muscle. This study highlights the importance of appropriate control of the gut microbiota and its metabolites, including butyric acid, for the optimum functioning of enteroendocrine cells.

Indexed as

Butyric AcidGlucagon-Like Peptide 1Lipid MetabolismReceptors, VasopressinAnimalsArginine VasopressinCell LineEnteroendocrine CellsGastrointestinal HormonesGastrointestinal MicrobiomeIntestinesMaleMiceMice, Inbred C57BLMice, KnockoutArginine VasopressinButyric AcidGastrointestinal HormonesGlucagon-Like Peptide 1Receptors, VasopressinArginine vasopressinButyric acidEnteroendocrine cellGlucagon-like peptide-1Lipid metabolism

Identifiers

PMID39668067
PMCPMC11728074

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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.