Goncalves Carolina G, Ramos Eduardo J B, Romanova Irina V, Suzuki Susumu, Chen Chung, Meguid Michael M
From the Surgical Metabolism and Nutrition Laboratory, Neuroscience Program, Department of Surgery.
Surgery. 2006 Feb;139(2):202-8. doi: 10.1016/j.surg.2005.08.001.
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.
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.
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.
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.
肿瘤生长会导致癌症厌食症,而使用ω-3脂肪酸(omega-3FA)可使其得到改善。我们推测,omega-3FA可调节荷瘤大鼠下丘脑促食欲神经肽Y(NPY)的上调以及厌食性α-黑素细胞刺激素(α-MSH)和5-羟色胺1B受体(5-HT(1B)-受体)的下调。
28只荷瘤大鼠分别喂食普通饲料(TB-对照)或omega-3FA(TB-omega-3FA)。当TB-对照大鼠出现厌食症时,将它们以及一组TB-omega-3大鼠处死。其余大鼠进行肿瘤切除(R-对照和R-omega-3FA),当厌食的TB-对照大鼠食物摄入量恢复正常时,取出大脑进行下丘脑免疫细胞化学研究,检测NPY、α-MSH和5-HT(1B)-受体抗体浓度。通过图像分析评估玻片之间的差异,并采用方差分析和t检验进行分析。
在厌食阶段,与TB-对照相比,TB-omega3FA组弓状核(ARC)的下丘脑NPY增加了38%,而ARC中的α-MSH减少了64%,室旁核(PVN)中的减少了29%。厌食阶段的omega-3FA饮食(TB-omega-3FA与R-omega-3FA相比)使ARC中的NPY产生了类似的定性变化(增加22%)和α-MSH(减少31%),同时PVN中的5-HT(1B)-受体减少了37%,证实了omega-3FA对下丘脑食物摄入调节因子的影响。然而,肿瘤切除后(TB-对照与R-对照相比),NPY增加了97%,α-MSH减少了62%,这一变化明显大于喂食omega-3FA饮食大鼠的变化。
肿瘤切除和omega-3FA可改变下丘脑食物摄入活动,上调NPY并下调α-MSH和5-HT(1B)-受体。与喂食omega3FA饮食的大鼠相比,喂食普通饲料的厌食大鼠进行肿瘤切除后,下丘脑NPY、α-MSH和食物摄入量在数量上恢复得更多。