M G Butler, M G Carlson, D E Schmidt, I D Feurer, T Thompson
{"title":"Prader-Willi综合征和肥胖受试者血浆胆囊收缩素水平。","authors":"M G Butler, M G Carlson, D E Schmidt, I D Feurer, T Thompson","doi":"10.1002/1096-8628(20001106)95:1<67::aid-ajmg13>3.0.co;2-k","DOIUrl":null,"url":null,"abstract":"<p><p>The cardinal feature of individuals with Prader-Willi syndrome (PWS) is severe hyperphagia-mediated obesity resulting from a faulty satiety mechanism. PWS is the most common genetic cause of marked obesity. Cholecystokinin (CCK) is a 33-amino-acid peptide found in high levels in the gut and brain involved in mediating the satiety response to meals. Free fatty acids (FFA) are responsible for the stimulation of CCK release after a fatty meal, and CCK and plasma FFA levels rise in tandem in normal individuals. Fasting plasma CCK levels were measured by radio-immunoassay in 33 PWS subjects with a mean age of 22.2 years +/- 8.1 years and 24 obese control subjects without a known cause of their obesity with a mean age of 28.7 years +/- 12.9 years. Consistent with previous findings, neither fasting plasma FFA levels (617.5 versus 486.8 microm/mL) or CCK levels (21.0 versus 19.1 pg/mL) were significantly different in PWS or control subjects, respectively. However, there was a significant correlation between fasting plasma FFA and CCK levels in obese subjects (r = 0. 64, P < 0.01), this correlation was completely lacking in PWS subjects (r = -0.06, P = 0.79). This difference in correlation coefficients constitutes a large effect. There were no significant effects observed for genetic subtypes (15q11-q13 deletion or maternal disomy 15), body mass index, percentage of fat, plasma levels of insulin, C-peptide, glucagon or leptin, age, or gender on CCK levels in our PWS subjects. These results suggest that differences in the peripheral CCK response to FFA levels may be a factor contributing to the altered satiety response in PWS subjects.</p>","PeriodicalId":7708,"journal":{"name":"American Journal of Medical Genetics","volume":"95 1","pages":"67-70"},"PeriodicalIF":0.0000,"publicationDate":"2000-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/1096-8628(20001106)95:1<67::aid-ajmg13>3.0.co;2-k","citationCount":"31","resultStr":"{\"title\":\"Plasma cholecystokinin levels in Prader-Willi syndrome and obese subjects.\",\"authors\":\"M G Butler, M G Carlson, D E Schmidt, I D Feurer, T Thompson\",\"doi\":\"10.1002/1096-8628(20001106)95:1<67::aid-ajmg13>3.0.co;2-k\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The cardinal feature of individuals with Prader-Willi syndrome (PWS) is severe hyperphagia-mediated obesity resulting from a faulty satiety mechanism. PWS is the most common genetic cause of marked obesity. Cholecystokinin (CCK) is a 33-amino-acid peptide found in high levels in the gut and brain involved in mediating the satiety response to meals. Free fatty acids (FFA) are responsible for the stimulation of CCK release after a fatty meal, and CCK and plasma FFA levels rise in tandem in normal individuals. Fasting plasma CCK levels were measured by radio-immunoassay in 33 PWS subjects with a mean age of 22.2 years +/- 8.1 years and 24 obese control subjects without a known cause of their obesity with a mean age of 28.7 years +/- 12.9 years. Consistent with previous findings, neither fasting plasma FFA levels (617.5 versus 486.8 microm/mL) or CCK levels (21.0 versus 19.1 pg/mL) were significantly different in PWS or control subjects, respectively. However, there was a significant correlation between fasting plasma FFA and CCK levels in obese subjects (r = 0. 64, P < 0.01), this correlation was completely lacking in PWS subjects (r = -0.06, P = 0.79). This difference in correlation coefficients constitutes a large effect. There were no significant effects observed for genetic subtypes (15q11-q13 deletion or maternal disomy 15), body mass index, percentage of fat, plasma levels of insulin, C-peptide, glucagon or leptin, age, or gender on CCK levels in our PWS subjects. These results suggest that differences in the peripheral CCK response to FFA levels may be a factor contributing to the altered satiety response in PWS subjects.</p>\",\"PeriodicalId\":7708,\"journal\":{\"name\":\"American Journal of Medical Genetics\",\"volume\":\"95 1\",\"pages\":\"67-70\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2000-11-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1002/1096-8628(20001106)95:1<67::aid-ajmg13>3.0.co;2-k\",\"citationCount\":\"31\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American Journal of Medical Genetics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/1096-8628(20001106)95:1<67::aid-ajmg13>3.0.co;2-k\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Medical Genetics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/1096-8628(20001106)95:1<67::aid-ajmg13>3.0.co;2-k","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 31
摘要
Prader-Willi综合征(PWS)患者的主要特征是由错误的饱腹机制引起的严重贪食介导的肥胖。PWS是显著肥胖最常见的遗传原因。胆囊收缩素(CCK)是一种由33个氨基酸组成的肽,在肠道和大脑中含量很高,参与调节对食物的饱腹感。游离脂肪酸(FFA)负责刺激脂肪餐后CCK的释放,在正常个体中,CCK和血浆FFA水平同步上升。采用放射免疫法测定33例PWS患者的空腹血浆CCK水平,平均年龄为22.2岁+/- 8.1岁,24例肥胖对照组,平均年龄为28.7岁+/- 12.9岁,肥胖原因不明。与先前的研究结果一致,空腹血浆FFA水平(617.5 vs 486.8 μ m/mL)和CCK水平(21.0 vs 19.1 pg/mL)在PWS和对照组中分别没有显著差异。然而,肥胖受试者空腹血浆FFA和CCK水平之间存在显著相关性(r = 0。64, P < 0.01), PWS患者完全没有这种相关性(r = -0.06, P = 0.79)。这种相关系数的差异构成了很大的影响。遗传亚型(15q11-q13缺失或母亲15型二体)、体重指数、脂肪百分比、血浆胰岛素、c肽、胰高血糖素或瘦素水平、年龄或性别对PWS受试者的CCK水平没有显著影响。这些结果表明,外周CCK对FFA水平的反应差异可能是导致PWS受试者饱腹感反应改变的一个因素。
Plasma cholecystokinin levels in Prader-Willi syndrome and obese subjects.
The cardinal feature of individuals with Prader-Willi syndrome (PWS) is severe hyperphagia-mediated obesity resulting from a faulty satiety mechanism. PWS is the most common genetic cause of marked obesity. Cholecystokinin (CCK) is a 33-amino-acid peptide found in high levels in the gut and brain involved in mediating the satiety response to meals. Free fatty acids (FFA) are responsible for the stimulation of CCK release after a fatty meal, and CCK and plasma FFA levels rise in tandem in normal individuals. Fasting plasma CCK levels were measured by radio-immunoassay in 33 PWS subjects with a mean age of 22.2 years +/- 8.1 years and 24 obese control subjects without a known cause of their obesity with a mean age of 28.7 years +/- 12.9 years. Consistent with previous findings, neither fasting plasma FFA levels (617.5 versus 486.8 microm/mL) or CCK levels (21.0 versus 19.1 pg/mL) were significantly different in PWS or control subjects, respectively. However, there was a significant correlation between fasting plasma FFA and CCK levels in obese subjects (r = 0. 64, P < 0.01), this correlation was completely lacking in PWS subjects (r = -0.06, P = 0.79). This difference in correlation coefficients constitutes a large effect. There were no significant effects observed for genetic subtypes (15q11-q13 deletion or maternal disomy 15), body mass index, percentage of fat, plasma levels of insulin, C-peptide, glucagon or leptin, age, or gender on CCK levels in our PWS subjects. These results suggest that differences in the peripheral CCK response to FFA levels may be a factor contributing to the altered satiety response in PWS subjects.