Evidence map›Paper›PMID 40603885›Full record

ArticleNPJ science of food2025

Water-soluble cellulose acetate attenuates glucose intolerance through GLP-1 and PYY signal upregulation.

Kohei Asaeda, Tomohisa Takagi, Eiki Murakami, Hikaru Hashimoto, Takeshi Yasuda, Mariko KajiwaraーKubota, Takeshi Sugaya, Katsura Mizushima, Yasuki Higashimura, Ohue-Kitano Ryuji and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NPJ science of food, 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

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

2 citing papers in PubMed.

  1. Review
  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

19 authors.

Kohei AsaedaDepartment of Gastroenterology, Kyoto Yamashiro General Medical Center, Kizugawa, Japan.
Tomohisa TakagiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan. takatomo@koto.kpu-m.ac.jp.
Eiki MurakamiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan.
Hikaru HashimotoDepartment of Gastroenterology, Osaka General Hospital of West Japan Railway Company, Osaka, Japan.
Takeshi YasudaDepartment of Gastroenterology, Akashi City Hospital, Akashi, Japan.
Mariko KajiwaraーKubotaDepartment of Gastroenterology, Fukuchiyama City Hospital, Fukuchiyama, Japan.
Takeshi SugayaDepartment of Gastroenterology, Dokkyo Medical University, Tochigi, Japan.
Katsura MizushimaDepartment of Human Immunology and Nutrition Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Yasuki HigashimuraDepartment of Food Science, Ishikawa Prefectural University, Nonoichi, Japan.
Ohue-Kitano RyujiDepartment of Biological and Environmental Chemistry, Kindai University, Higashiosaka, Japan.
Ikuo KimuraLaboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
Ken InoueDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan.
Kazuhiko UchiyamaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan.
Shu ShimamotoDaicel Corporation, R&D Headquarters, Tokyo, Japan.
Yuichi UkawaDaicel Corporation, R&D Headquarters, Tokyo, Japan.
Akiko KoharaDaicel Corporation, Healthcare SBU, Tokyo, Japan.
Masatake KudohDaicel Corporation, Healthcare SBU, Niigata, Japan.
Yuji NaitoDepartment of Human Immunology and Nutrition Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Yoshito ItohDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan.

Funding

Grant-in-Aid for Scientific Research (KAKENHI) (C) 24K11092
6 · The paper itself

Abstract

Water-soluble cellulose acetate (WSCA), derived from natural cellulose and acetate, can be used as a food additive and deliver acetate to the large intestine. In this study, we investigated the effects of dietary WSCA supplementation on impaired glucose metabolism in db/db mice, a model of type 2 diabetes mellitus. db/m and db/db mice were fed either a control diet or a WSCA-supplemented diet for eight weeks. The WSCA-supplemented group exhibited improved glucose intolerance or lipid metabolism without any loss of skeletal muscle mass or grip strength. WSCA supplementation significantly increased acetate concentrations in the cecum, stool, and blood. Furthermore, serum levels of glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) were significantly higher in the WSCA group than in the control group. These findings suggest that WSCA delivers acetate to the colon and prevents diabetes by enhancing GLP-1 and PYY secretion in db/db mice.

Identifiers

PMID40603885
PMCPMC12222533

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.