不同肿瘤患者leptin与NPY关系的研究

目的：探讨胃癌等肿瘤患者瘦素（leptin）与神经肽Y（neuropeptide，NPY）的相互关系。方法：应用放射免疫分析测定180例不同肿瘤患者血清leptin和血浆NPY水平，并与30例正常人作比较。结果：①leptin水平与对照组（4．18±0．51ng／m1）比较，胃癌、肝癌、食管癌、直、结肠癌和肺癌组均明显增高，并具显著性差异（P〈0．01；P〈0．05；P〈0．01；P〈0．01；P〈0．05）。正常对照组血浆NPY水平为（150．25±20．33）pg／ml，除肝癌组外，其它各恶性肿瘤组血浆NPY水平均较对照组增高显著。②相关分析显示，胃癌、食管癌、直肠癌患者lepdn浓度增高与NPY增高呈明显正相关，其r值分别为0．354、0．30、0．285，P值均〈0．01。胃癌、肝癌、食管癌、直肠癌leptin与TG之间呈明显正相关，其r值分别为0．301、0．268、0．335，P值均〈0．01；leptin与TC、LDL—C、HDL—C之间无相关性。结论：①胃癌等肿瘤患者存在着高leptin和NPY血症；③leptin、NPY在恶性肿瘤食欲及能量调节过程中合成、分泌、与受体结合力的异常在肿瘤恶病质的形成中发挥重要作用。

Relationship Between Leptin and Neuropeptide Y Levels in Patients with Different Kinds of Tumors

Objective To investigate the relationship between leptin and neuropeptide Y （N-PY） levels in patients with different kinds of tumors. Methods Serum leptin and plasma NPY levels were between with RIA in 180 patients with different kinds of tumors and 30 controls. Results ① Leptin levels were statistically higher in patients with gastric cancer （ n = 38）, liver cancer （ n = 30）, esophageal carcinoma （ n = 38 ） , colon carcinoma （ n = 32 ） and lung cancer （ n = 42） than those in controls （ 4.18 ± 0.51 ng/ml ） （ P 〈 0. 01, P 〈 0.05, P 〈 0. 01, P 〈 0. 01, P 〈 0.05 ）. Plasma NPY levels in controls were （ 150.25 ± 20.33 ） pg/ml. NPY levels were significantly higher in the patients （ except patients with liver cancer than those in controls）. ③ Leptin levels were positively correlated with NPY levels in patients with gastric cancer. Esophageal carcinoma and colon carcinoma （ r = 0. 354, 0. 30, 0. 285, P 〈 0.01 ）. Leptin levels were also positively correlated with TG in patients with gastric cancer, liver cancer, esophageal carcinoma and colon carcinoma （ r = 0. 301,0. 268, 0. 335, P 〈 0. 01 ）. There were no correlations between leptin and TC, LDL - C, HDL - C levels. Conclusion ① There were high leptin and NPY blood levels in patients with gastric cancer, liver cancer, esophagesl carcinoma, colon carcinoma, and lung cancer. ②Leptin and NPY might play important roles in the development of tumor cachexia through their abnormal synthesis, secretion and receptor binding.