Evidence map›Paper›PMID 26136415›Full record

ArticleJournal of cachexia, sarcopenia and muscle2015

Differences in food intake of tumour-bearing cachectic mice are associated with hypothalamic serotonin signalling.

Jvalini T Dwarkasing, Mark V Boekschoten, Joseph M Argilès, Miriam van Dijk, Silvia Busquets, Fabio Penna, Miriam Toledo, Alessandro Laviano, R F Witkamp, Klaske van Norren

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

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  13. Liquid Biopsy for Cancer Cachexia: Focus on Muscle-Derived microRNAs.International journal of molecular sciences · 2021
    Review
  14. Review
  15. Review
  16. Cachexia, a Systemic Disease beyond Muscle Atrophy.International journal of molecular sciences · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. Inter-tissue communication in cancer cachexia.Nature reviews. Endocrinology · 2018
    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

10 authors at 4 institutions in 3 countries.

Jvalini T DwarkasingNutrition and Pharmacology Group, Division of Human Nutrition, Wageningen University, Wageningen, The Netherlands.
Mark V BoekschotenNutrition, Metabolism and Genomics Group, Division of Human Nutrition, Wageningen University, Wageningen, The Netherlands.
Joseph M ArgilèsCancer Research Group, Departament de Bioquímica i Biologia Molecular, University of Barcelona, Barcelona, Spain.
Miriam van DijkNutricia Research, Utrecht, The Netherlands.
Silvia BusquetsCancer Research Group, Departament de Bioquímica i Biologia Molecular, University of Barcelona, Barcelona, Spain.
Fabio PennaCancer Research Group, Departament de Bioquímica i Biologia Molecular, University of Barcelona, Barcelona, Spain.
Miriam ToledoCancer Research Group, Departament de Bioquímica i Biologia Molecular, University of Barcelona, Barcelona, Spain.
Alessandro LavianoDepartment of Clinical Medicine, Sapienza University, Rome, Italy.
R F WitkampNutrition and Pharmacology Group, Division of Human Nutrition, Wageningen University, Wageningen, The Netherlands.
Klaske van NorrenNutrition and Pharmacology Group, Division of Human Nutrition, Wageningen University, Wageningen, The Netherlands.
Universitat de Barcelona · ESWageningen University & Research · NLNutricia Research (Netherlands) · NLSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnorexia is a common symptom among cancer patients and contributes to malnutrition and strongly impinges on quality of life. Cancer-induced anorexia is thought to be caused by an inability of food intake-regulating systems in the hypothalamus to respond adequately to negative energy balance during tumour growth. Here, we show that this impaired response of food-intake control is likely to be mediated by altered serotonin signalling and by failure in post-transcriptional neuropeptide Y (NPY) regulation.

methodsTwo tumour cachectic mouse models with different food intake behaviours were used: a C26-colon adenocarcinoma model with increased food intake and a Lewis lung carcinoma model with decreased food intake. This contrast in food intake behaviour between tumour-bearing (TB) mice in response to growth of the two different tumours was used to distinguish between processes involved in cachexia and mechanisms that might be important in food intake regulation. The hypothalamus was used for transcriptomics (affymetrix chips).

resultsIn both models, hypothalamic expression of orexigenic NPY was significantly higher compared with controls, suggesting that this change does not directly reflect food intake status but might be linked to negative energy balance in cachexia. Expression of genes involved in serotonin signalling showed to be different between C26-TB mice and Lewis lung carcinoma-TB mice and was inversely associated with food intake. In vitro, using hypothalamic cell lines, serotonin repressed neuronal hypothalamic NPY secretion while not affecting messenger NPY expression, suggesting that serotonin signalling can interfere with NPY synthesis, transport, or secretion.

conclusionsAltered serotonin signalling is associated with changes in food intake behaviour in cachectic TB mice. Serotonins' inhibitory effect on food intake under cancer cachectic conditions is probably via affecting the NPY system. Therefore, serotonin regulation might be a therapeutic target to prevent the development of cancer-induced eating disorders.

Indexed as

AnorexiaCachexiaCancerNeuropeptide YSerotonin

Identifiers

PMID26136415
PMCPMC4435100
OpenAlexW2164157560

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.