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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
Published on: November 30, 2016
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Hypothalamic food intake regulation in a cancer-cachectic mouse model
Jvalini T Dwarkasing1, Miriam van Dijk, Francina J Dijk
1Nutrition and Pharmacology Group, Division of Human Nutrition, Wageningen University, Bomenweg 2, 6703, Wageningen, The Netherlands.
Journal of Cachexia, Sarcopenia and Muscle
|November 14, 2013
Summary
Cancer cachexia in mice paradoxically increases food intake, altering hypothalamic gene expression. Key appetite regulators like NPY, AgRP, and serotonin signaling pathways are significantly changed, offering potential therapeutic targets for eating disorders.
Area of Science:
- Neuroscience
- Oncology
- Metabolism
Background:
- Cancer patients often experience appetite loss (anorexia) and insufficient food intake.
- This study investigates a mouse model of cancer cachexia exhibiting increased food intake despite body weight loss.
- Understanding hypothalamic appetite regulation in this model may reveal targets for treating cancer-induced eating disorders.
Purpose of the Study:
- To analyze the hypothalamic gene expression profile in a mouse model of cancer cachexia with increased food intake.
- To identify alterations in appetite-regulating systems within the hypothalamus during tumor growth.
- To explore potential therapeutic targets for cancer-related eating disorders.
Main Methods:
- Subcutaneous inoculation of C26 colon adenocarcinoma cells in male CDF1 mice.
- Monitoring of body weight and food intake throughout the study.
- Transcriptomic analysis of the hypothalamus using Affymetrix chips on day 20 post-inoculation.
Main Results:
- Tumor-bearing mice showed increased food intake and body weight loss.
- Upregulation of orexigenic neuropeptides (NPY, AgRP) and downregulation of anorexigenic genes (CCK, POMC) in the hypothalamus.
- Significant alterations in serotonin and dopamine signaling pathways, with lower brain serotonin levels correlating inversely with food intake.
Conclusions:
- Transcriptomic analysis revealed changes in NPY, AgRP, and serotonin signaling in the hypothalamus of cachectic mice with increased food intake.
- Brain serotonin levels correlate with observed changes in food intake.
- Further research is needed to determine if targeting these systems can prevent cancer-induced eating disorders.
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