Evidence map›Paper›PMID 35068677›Full record

ArticleJournal of clinical biochemistry and nutrition2022

Treatment with broad-spectrum antibiotics upregulates Sglt1 and induces small intestinal villous hyperplasia in mice.

Takayuki Ota, Takeshi Ishikawa, Tomoki Sakakida, Yuki Endo, Shinya Matsumura, Juichirou Yoshida, Yasuko Hirai, Katsura Mizushima, Kaname Oka, Toshifumi Doi and 8 more

Open access · diamondAbstract read
In one paragraph

Article in Journal of clinical biochemistry and nutrition, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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

18 authors at 1 institution in 1 country.

Takayuki OtaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Takeshi IshikawaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Tomoki SakakidaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Yuki EndoMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Shinya MatsumuraMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Juichirou YoshidaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Yasuko HiraiMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Katsura MizushimaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Kaname OkaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Toshifumi DoiMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Tetsuya OkayamaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Ken InoueMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Kazuhiro KamadaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Kazuhiko UchiyamaMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Tomohisa TakagiMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Hideyuki KonishiMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Yuji NaitoMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Yoshito ItohMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Hirokoji Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Kyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although extensive evidence indicates that the gut microbiota plays a crucial role in regulating glucose homeostasis, the exact regulatory mechanism remains unclear. This study aimed to investigate the effect of broad-spectrum antibiotics on the expression of glucose transporters, histomorphology of the small intestine, and glucose metabolism in mice. C57BL/6 mice were administered drinking water with or without a broad-spectrum antibiotic combination for 4 weeks. Thereafter, an oral glucose tolerance test was performed. Body weight, small intestine histopathology, mRNA levels of glucose transporters (SGLT1 and GLUT2) and intestinal transcription factors (CDX1 and CDX2) were evaluated. SGLT1 and CDX1 were upregulated in the small intestine upon antibiotic administration compared with that in the control group. The height and surface area of the jejunal villi were significantly higher upon antibiotic administration than in the control group. Fasting glucose levels were significantly higher upon antibiotic administration than in the control group. The present results indicate that treatment with broad-spectrum antibiotics upregulates SGLT1 and CDX1 and induces hyperplasia in the small intestine, thus increasing fasting blood glucose levels. Our results further the current understanding of the effects of broad-spectrum antibiotics on the gut microbiota and glucose homeostasis that may have future clinical implications.

Indexed as

antibioticsglucose tolerancegut microbiotaintestinal hyperplasiaSGLT1

Identifiers

PMID35068677
PMCPMC8764108
OpenAlexW3185910169

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LicenceCC BY-NC-ND
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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.