title: Omega-3 fatty acids improve appetite in cancer anorexia, but tumor resecting restores it.
abstract: BACKGROUND
  Tumor growth leads to cancer anorexia that is ameliorated using omega-3 fatty acids (omega-3FA). We hypothesize that omega-3FA modulates up-regulation of hypothalamic orexigenic neuropeptide Y (NPY) and down-regulation of anorexigenic alpha melanocyte-stimulating hormone (alpha-MSH) and serotonin 1B receptors (5-HT(1B)-receptors) in tumor-bearing rats.
  
  
  METHODS
  Twenty-eight tumor-bearing rats were fed either chow (TB-Control) or omega-3FA (TB-omega-3FA). When anorexia developed in TB-Control rats, they and a cohort of TB-omega-pi-3 rats were killed. The rest had their tumor resected (R-Control and R-omega-3FA), and when anorexic TB-Controls normalized their food intake, brains were removed for hypothalamic immunocytochemical study of NPY, alpha-MSH, and 5-HT(1B)-receptor antibodies concentrations. Comparison among slides were assessed by image analysis and analyzed by ANOVA and t test.
  
  
  RESULTS
  At anorexia, hypothalamic NPY in arcuate nucleus (ARC) increased by 38% in TB-omega3FA versus TB-Control, whereas alpha-MSH decreased 64% in ARC and 29% in paraventricular nucleus (PVN). Omega-3FA diet in anorexia (TB-omega-3FA vs R-omega-3FA) produced similar qualitative changes of NPY (22% increase) and alpha-MSH (31% decrease) in ARC, with concomitant decrease of 37% in 5-HT(1B)-receptors in PVN, confirming the influence of omega-3FA on the hypothalamic food intake modulators. However, after tumor resection (TB-Control vs R-Control) a 97% increase in NPY and a 62% decrease in alpha-MSH occurred that was significantly greater than in rats fed omega-3FA diet.
  
  
  CONCLUSIONS
  Tumor resection and omega-3FA modifies hypothalamic food intake activity, up-regulating NPY and down-regulating alpha-MSH and 5-HT(1B)-receptors. Tumor resection in anorexic rats on chow diet restored hypothalamic NPY, alpha-MSH, and food intake quantitatively more than in rats fed omega3FA diet.
authors.affiliation: From the Surgical Metabolism and Nutrition Laboratory, Neuroscience Program, Department of Surgery.
authors.forename: Carolina G
authors.initials: CG
authors.lastname: Goncalves
authors.forename: Eduardo J B
authors.initials: EJ
authors.lastname: Ramos
authors.forename: Irina V
authors.initials: IV
authors.lastname: Romanova
authors.forename: Susumu
authors.initials: S
authors.lastname: Suzuki
authors.forename: Chung
authors.initials: C
authors.lastname: Chen
authors.forename: Michael M
authors.initials: MM
authors.lastname: Meguid
mesh_terms: D000821:Animal Feed; D000818:Animals; D000855:Anorexia / Q000188:drug therapy* / Q000209:etiology*; D001066:Appetite / Q000187:drug effects*; D015536:Down-Regulation; D004435:Eating; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology*; D007031:Hypothalamus / Q000502:physiology; D008297:Male; D009369:Neoplasms / Q000150:complications / Q000601:surgery; D009478:Neuropeptide Y / Q000096:biosynthesis; D051381:Rats; D011916:Rats, Inbred F344; D044302:Receptor, Serotonin, 5-HT1B / Q000096:biosynthesis; D015854:Up-Regulation
chemical_list: D015525:Fatty Acids, Omega-3; D009478:Neuropeptide Y; D044302:Receptor, Serotonin, 5-HT1B