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Tumor growth leads to cancer anorexia that is ameliorated using omega-3 fatty acids (ϖ-3FA). We hypothesize that ϖ-3FA modulates up-regulation of hypothalamic orexigenic neuropeptide Y (NPY) and down-regulation of anorexigenic alpha melanocyte–stimulating hormone (α-MSH) and serotonin 1B receptors (5-HT1B-receptors) in tumor-bearing rats.Twenty-eight tumor-bearing rats were fed either chow (TB-Control) or ϖ-3FA (TB-ϖ-3FA). When anorexia developed in TB-Control rats, they and a cohort of TB-ϖ-3 rats were killed. The rest had their tumor resected (R-Control and R-ϖ-3FA), and when anorexic TB-Controls normalized their food intake, brains were removed for hypothalamic immunocytochemical study of NPY, α-MSH, and 5-HT1B-receptor antibodies concentrations. Comparison among slides were assessed by image analysis and analyzed by ANOVA and t test.At anorexia, hypothalamic NPY in arcuate nucleus (ARC) increased by 38% in TB-ϖ-3FA versus TB-Control, whereas α-MSH decreased 64% in ARC and 29% in paraventricular nucleus (PVN). Omega-3FA diet in anorexia (TB-ϖ-3FA vs R-ϖ-3FA) produced similar qualitative changes of NPY (22% increase) and α-MSH (31% decrease) in ARC, with concomitant decrease of 37% in 5-HT1B-receptors in PVN, confirming the influence of ϖ-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 α-MSH occurred that was significantly greater than in rats fed ϖ-3FA diet.Tumor resection and ϖ-3FA modifies hypothalamic food intake activity, up-regulating NPY and down-regulating α-MSH and 5-HT1B-receptors. Tumor resection in anorexic rats on chow diet restored hypothalamic NPY, α-MSH, and food intake quantitatively more than in rats fed ϖ-3FA diet.