Evidence map›Paper›PMID 26892894›Full record

ArticleScientific reports2016

Long-term High Fat Ketogenic Diet Promotes Renal Tumor Growth in a Rat Model of Tuberous Sclerosis.

Arkadiusz D Liśkiewicz, Daniela Kasprowska, Anna Wojakowska, Krzysztof Polański, Joanna Lewin-Kowalik, Katarzyna Kotulska, Halina Jędrzejowska-Szypułka

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.

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  19. Metabolic reprogramming in prostate cancer.British journal of cancer · 2021
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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

7 authors at 4 institutions in 2 countries.

Arkadiusz D LiśkiewiczMedical University of Silesia, School of Medicine in Katowice, Department of Physiology, Katowice, Poland.
Daniela KasprowskaMedical University of Silesia, School of Medicine in Katowice, Department of Pharmacology, Katowice, Poland.
Anna WojakowskaMaria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Gliwice Branch, Poland.
Krzysztof PolańskiWarwick Systems Biology Centre, University of Warwick, CV4 7AL, UK.
Joanna Lewin-KowalikMedical University of Silesia, School of Medicine in Katowice, Department of Physiology, Katowice, Poland.
Katarzyna KotulskaDepartment of Neurology and Epileptology, The Children's Memorial Health Institute, Warsaw, Poland.
Halina Jędrzejowska-SzypułkaMedical University of Silesia, School of Medicine in Katowice, Department of Physiology, Katowice, Poland.
Medical University of Silesia · PLChildren's Memorial Health Institute · PLThe Maria Sklodowska-Curie National Research Institute of Oncology · PLUniversity of Warwick · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nutritional imbalance underlies many disease processes but can be very beneficial in certain cases; for instance, the antiepileptic action of a high fat and low carbohydrate ketogenic diet. Besides this therapeutic feature it is not clear how this abundant fat supply may affect homeostasis, leading to side effects. A ketogenic diet is used as anti-seizure therapy i.a. in tuberous sclerosis patients, but its impact on concomitant tumor growth is not known. To examine this we have evaluated the growth of renal lesions in Eker rats (Tsc2+/-) subjected to a ketogenic diet for 4, 6 and 8 months. In spite of existing opinions about the anticancer actions of a ketogenic diet, we have shown that this anti-seizure therapy, especially in its long term usage, leads to excessive tumor growth. Prolonged feeding of a ketogenic diet promotes the growth of renal tumors by recruiting ERK1/2 and mTOR which are associated with the accumulation of oleic acid and the overproduction of growth hormone. Simultaneously, we observed that Nrf2, p53 and 8-oxoguanine glycosylase α dependent antitumor mechanisms were launched by the ketogenic diet. However, the pro-cancerous mechanisms finally took the ascendency by boosting tumor growth.

Indexed as

AnimalsCarcinoma, Renal CellDiet, High-FatDiet, KetogenicDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesFemaleInsulinInsulin-Like Growth Factor IKidneyKidney NeoplasmsMaleOleic AcidRats, Long-EvansTOR Serine-Threonine KinasesTuberous SclerosisExtracellular Signal-Regulated MAP KinasesInsulininsulin-like growth factor-1, ratInsulin-Like Growth Factor ImTOR protein, ratOleic AcidTOR Serine-Threonine Kinases

Identifiers

PMID26892894
PMCPMC4759602
OpenAlexW2415998167

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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.