{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T10:09:16Z","timestamp":1792145356554,"version":"4.4.0"},"reference-count":51,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2015,3,31]],"date-time":"2015-03-31T00:00:00Z","timestamp":1427760000000},"content-version":"vor","delay-in-days":30,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"name":"European Union's Seventh Framework Programme","award":["266408"],"award-info":[{"award-number":["266408"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2015,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Anorexia is a common symptom among cancer patients and contributes to malnutrition and strongly impinges on quality of life. Cancer\u2010induced anorexia is thought to be caused by an inability of food intake\u2010regulating systems in the hypothalamus to respond adequately to negative energy balance during tumour growth. Here, we show that this impaired response of food\u2010intake control is likely to be mediated by altered serotonin signalling and by failure in post\u2010transcriptional neuropeptide Y (NPY) regulation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Two tumour cachectic mouse models with different food intake behaviours were used: a C26\u2010colon adenocarcinoma model with increased food intake and a Lewis lung carcinoma model with decreased food intake. This contrast in food intake behaviour between tumour\u2010bearing (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).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In 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\u2010TB mice and Lewis lung carcinoma\u2010TB mice and was inversely associated with food intake. <jats:italic>In vitro<\/jats:italic>, 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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Altered 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\u2010induced eating disorders.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcsm.12008","type":"journal-article","created":{"date-parts":[[2015,4,1]],"date-time":"2015-04-01T09:26:32Z","timestamp":1427880392000},"page":"84-94","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":51,"title":["Differences in food intake of tumour\u2010bearing cachectic mice are associated with hypothalamic serotonin signalling"],"prefix":"10.1002","volume":"6","author":[{"given":"Jvalini T.","family":"Dwarkasing","sequence":"first","affiliation":[{"name":"Nutrition and Pharmacology Group, Division of Human Nutrition Wageningen University  Wageningen The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark V.","family":"Boekschoten","sequence":"additional","affiliation":[{"name":"Nutrition, Metabolism and Genomics Group, Division of Human Nutrition Wageningen University  Wageningen The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph M.","family":"Argil\u00e8s","sequence":"additional","affiliation":[{"name":"Cancer Research Group, Departament de Bioqu\u00edmica i Biologia Molecular University of Barcelona  Barcelona Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miriam","family":"van Dijk","sequence":"additional","affiliation":[{"name":"Nutricia Research  Utrecht The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silvia","family":"Busquets","sequence":"additional","affiliation":[{"name":"Cancer Research Group, Departament de Bioqu\u00edmica i Biologia Molecular University of Barcelona  Barcelona Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabio","family":"Penna","sequence":"additional","affiliation":[{"name":"Cancer Research Group, Departament de Bioqu\u00edmica i Biologia Molecular University of Barcelona  Barcelona Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miriam","family":"Toledo","sequence":"additional","affiliation":[{"name":"Cancer Research Group, Departament de Bioqu\u00edmica i Biologia Molecular University of Barcelona  Barcelona Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessandro","family":"Laviano","sequence":"additional","affiliation":[{"name":"Department of Clinical Medicine Sapienza University  Rome Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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