Evidence map›Paper›PMID 37679316›Full record

ArticleCell death & disease2023

Metabolic intervention by low carbohydrate diet suppresses the onset and progression of neuroendocrine tumors.

Yu Chen, Tatsuki Yamamoto, Yura Takahashi, Tomoka Moro, Tomoko Tajima, Yukiko Sakaguchi, Naoaki Sakata, Akihiko Yokoyama, Susumu Hijioka, Akane Sada and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

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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

12 authors at 5 institutions in 2 countries.

Yu ChenLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Tatsuki YamamotoLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Yura TakahashiLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Tomoka MoroLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Tomoko TajimaLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Yukiko SakaguchiLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Naoaki SakataDepartment of Regenerative Medicine and Transplantation, Faculty of Medicine, Fukuoka University, Nanakuma 7-45-1, Jonan-ku, Fukuoka, 814-0180, Japan.ORCID 0000-0002-3495-4270
Akihiko YokoyamaTsuruoka Metabolomics Laboratory, National Cancer Center, Yamagata, 997-0052, Japan.ORCID 0000-0002-5639-8068
Susumu HijiokaDepartment of Hepatobiliary and Pancreatic Oncology, National Cancer Center Hospital, Tokyo, 104-0045, Japan.
Akane SadaLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Yuko TabataLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Rieko OhkiLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan. rohki@ncc.go.jp.ORCID 0000-0002-7775-6653
Tokyo Institute of Psychiatry · JPChiba University · JPFukuoka University · JPNational Cancer Research Institute · GBNational Institute of Technology, Tsuruoka College · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin signaling often plays a role in the regulation of cancer, including tumor initiation, progression, and response to treatment. In addition, the insulin-regulated PI3K-Akt-mTOR pathway plays an important role in the regulation of islet cell proliferation, and this pathway is hyperactivated in human non-functional pancreatic neuroendocrine tumors (PanNETs). We, therefore, investigated the effect of a very low carbohydrate diet (ketogenic diet) on a mouse model that develops non-functional PanNETs to ask how reduced PI3K-Akt-mTOR signaling might affect the development and progression of non-functional PanNET. We found that this dietary intervention resulted in lower PI3K-Akt-mTOR signaling in islet cells and a significant reduction in PanNET formation and progression. We also found that this treatment had a significant effect on the suppression of pituitary NET development. Furthermore, we found that non-functional PanNET patients with lower blood glucose levels tend to have a better prognosis than patients with higher blood glucose levels. This preclinical study shows that a dietary intervention that results in lower serum insulin levels leads to lower insulin signals within the neuroendocrine cells and has a striking suppressive effect on the development and progression of both pancreatic and pituitary NETs.

Indexed as

Neuroendocrine TumorsAnimalsBlood GlucoseDiet, Carbohydrate-RestrictedHumansInsulinMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor Protein-Tyrosine KinasesTOR Serine-Threonine KinasesBlood GlucoseInsulinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor Protein-Tyrosine KinasesTOR Serine-Threonine Kinases

Identifiers

PMID37679316
PMCPMC10484927
OpenAlexW4386517386

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.