Baranowska B, Radzikowska M, Wasilewska-Dziubińska E, Kapliński A, Roguski K, Płonowski A
Neuroendocrinology Department, Medical Centre of Postgraduate Education, Warsaw, Poland.
Gynecol Endocrinol. 1999 Oct;13(5):344-51. doi: 10.3109/09513599909167578.
It has been reported that polycystic ovary syndrome (PCOS) is very frequently associated with obesity, insulin resistance and hyperinsulinemia. However, metabolic disorders may lead to suppression of reproductive hormone secretion during undernutrition and in obesity. Some neuropeptides, such as neuropeptide Y (NPY) and galanin, modulate the control of appetite and play an important role in the mechanism of luteinizing hormone-releasing hormone (LHRH) secretion. NPY and galanin regulate appetite via both central and peripheral mechanisms. The interaction between central and peripheral signals for the control of food intake is due to leptin. Leptin can modulate the activity of NPY and other peptides in the hypothalamus that are known to affect eating behavior. In order to evaluate the relationship between NPY, galanin and leptin, 28 women with PCOS, 32 obese women (non-PCOS) and 19 lean healthy women (control group) were investigated. Obese women with PCOS were divided into two groups: PCOS (A) overweight (body mass index, BMI 26-30 kg/m2), and PCOS (B) obese (BMI 31-40 kg/m2). Plasma NPY, galanin and leptin concentrations were measured by radioimmunoassay. Plasma leptin levels in obese women with PCOS (groups A and B) were significantly higher than those in the control group (p < 0.05, p < 0.05, respectively). A significant positive correlation between plasma leptin and BMI in women with PCOS was found (r = 0.427, p < 0.01). A positive correlation was demonstrated between leptin and testosterone in PCOS (r = 0.461, p < 0.01). Plasma galanin concentrations in PCOS were higher than in the control group but the differences were not significant. Plasma NPY levels were significantly elevated in both non-obese (normal) and obese women with PCOS (group A) (p < 0.01, p < 0.005, respectively). However, in obese non-PCOS women plasma NPY levels gradually increased with increase in BMI. No significant correlations were found between galanin, NPY and percentage change in response of LH to LHRH, as well as between NPY and insulin, and galanin and testosterone. Plasma insulin concentrations in women with PCOS (group B) were significantly higher than in the control group (p < 0.001). Increased plasma NPY levels are found in both obese and non-obese women with PCOS. The increase in NPY is independent of the increase in BMI. In obese women with PCOS, plasma leptin is increased compared with control lean women. Serum insulin concentration is increased in obese women with PCOS. A positive correlation exists between leptin and BMI as well as between leptin and testosterone in women with PCOS. These results may suggest that the feedback system in the interaction between leptin and NPY is disturbed in PCOS.
据报道，多囊卵巢综合征（PCOS）常与肥胖、胰岛素抵抗和高胰岛素血症相关。然而，代谢紊乱可能在营养不良和肥胖期间导致生殖激素分泌受到抑制。一些神经肽，如神经肽Y（NPY）和甘丙肽，可调节食欲控制，并在促黄体生成素释放激素（LHRH）分泌机制中发挥重要作用。NPY和甘丙肽通过中枢和外周机制调节食欲。食物摄入控制中中枢和外周信号之间的相互作用归因于瘦素。瘦素可调节下丘脑中已知会影响进食行为的NPY和其他肽的活性。为了评估NPY、甘丙肽和瘦素之间的关系，对28名PCOS女性、32名肥胖女性（非PCOS）和19名健康瘦女性（对照组）进行了研究。患有PCOS的肥胖女性分为两组：PCOS（A）超重（体重指数，BMI 26 - 30 kg/m²），以及PCOS（B）肥胖（BMI 31 - 40 kg/m²）。通过放射免疫测定法测量血浆NPY、甘丙肽和瘦素浓度。患有PCOS的肥胖女性（A组和B组）的血浆瘦素水平显著高于对照组（分别为p < 0.05，p < 0.05）。发现PCOS女性血浆瘦素与BMI之间存在显著正相关（r = 0.427，p < 0.01）。PCOS患者中瘦素与睾酮之间存在正相关（r = 0.461，p < 0.01）。PCOS患者的血浆甘丙肽浓度高于对照组，但差异不显著。非肥胖（正常）和肥胖的PCOS女性（A组）的血浆NPY水平均显著升高（分别为p < 0.01，p < 0.005）。然而，在肥胖的非PCOS女性中，血浆NPY水平随BMI增加而逐渐升高。未发现甘丙肽、NPY与LH对LHRH反应的百分比变化之间，以及NPY与胰岛素、甘丙肽与睾酮之间存在显著相关性。患有PCOS的女性（B组）的血浆胰岛素浓度显著高于对照组（p < 0.001）。肥胖和非肥胖的PCOS女性均发现血浆NPY水平升高。NPY的升高与BMI的增加无关。在患有PCOS的肥胖女性中，与对照瘦女性相比，血浆瘦素升高。患有PCOS的肥胖女性血清胰岛素浓度升高。PCOS女性中瘦素与BMI以及瘦素与睾酮之间存在正相关。这些结果可能表明，PCOS中瘦素与NPY相互作用的反馈系统受到干扰。
