Correlation between fasting plasma ghrelin levels and age, body mass index (BMI), BMI percentiles, and 24-hour plasma ghrelin profiles in Prader-Willi syndrome

被引:44
作者
Paik, KH
Jin, DK
Song, SY
Lee, JE
Ko, SH
Song, SM
Kim, JS
Oh, YJ
Kim, SW
Lee, SH
Kim, SH
Kwon, EK
Choe, YH
机构
[1] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pediat, Seoul 135710, South Korea
[2] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, Seoul 135710, South Korea
[3] Samsung Biomed Res Inst, Clin Res Ctr, Seoul 135710, South Korea
[4] Inha Univ, Coll Med, Dept Pediat, Inchon 400711, South Korea
关键词
D O I
10.1210/jc.2003-032137
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Ghrelin is a GH-releasing acylated peptide found in the stomach and a centrally acting food intake stimulator. Prader-Willi syndrome (PWS) is a genetic disorder characterized by a voracious appetite and increased fasting ghrelin levels. In this report we describe 24-h ghrelin profiles in PWS children (n = 5) and compare these with age, sex, and body mass index (BMI)-matched controls (n = 5). A 3- to 4-fold increase in ghrelin levels was found in PWS over a 24-h period, compared with controls (P < 0.001). Interestingly, there was a greater tendency for the up-regulation of ghrelin level in lean PWS than in obese PWS. To confirm this finding, we measured fasting ghrelin levels in 39 patients with PWS. Inverse correlations were found between plasma ghrelin levels and the following: age (r = -0.408, P = 0.005), BMI (r = -0.341, P = 0.017), percentage of the ideal weight for age (r = -0.382, P = 0.008), and BMI percentile (r = -0.311, P = 0.027). Our data show that there may be a suppressive (or up-regulating) controlling mechanism of ghrelin secretion in obese ( or lean) PWS children. We hope that our data may further explain the mechanisms underlying the insatiable appetite and obesity characteristic of PWS.
引用
收藏
页码:3885 / 3889
页数:5
相关论文
共 20 条
[1]   Ghrelin secretion in humans is sexually dimorphic, suppressed by somatostatin, and not affected by the ambient growth hormone levels [J].
Barkan, AL ;
Dimaraki, EV ;
Jessup, SK ;
Symons, KV ;
Ermolenko, M ;
Jaffe, CA .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2003, 88 (05) :2180-2184
[2]  
Bueno G, 2000, J PEDIATR ENDOCR MET, V13, P425
[3]  
Butler MG, 1998, AM J MED GENET, V75, P7, DOI 10.1002/(SICI)1096-8628(19980106)75:1<7::AID-AJMG3>3.0.CO
[4]  
2-T
[5]   Elevated plasma ghrelin levels in Prader-Willi syndrome [J].
Cummings, DE ;
Clement, K ;
Purnell, JQ ;
Vaisse, C ;
Foster, KE ;
Frayo, RS ;
Schwartz, MW ;
Basdevant, A ;
Weigle, DS .
NATURE MEDICINE, 2002, 8 (07) :643-644
[6]   High circulating ghrelin:: A potential cause for hyperphagia and obesity in Prader-Willi syndrome [J].
DelPparigi, A ;
Tschöp, M ;
Heiman, ML ;
Salbe, AD ;
Vozarova, B ;
Sell, SM ;
Bunt, JC ;
Tataranni, PA .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (12) :5461-5464
[7]   Body fat determined by skinfold measurements is elevated despite underweight in infants with Prader-Labhart-Willi syndrome [J].
Eiholzer, U ;
Blum, WF ;
Molinari, L .
JOURNAL OF PEDIATRICS, 1999, 134 (02) :222-225
[8]   Is there growth hormone deficiency in Prader-Willi syndrome? - Six arguments to support the presence of hypothalamic growth hormone deficiency in Prader-Willi syndrome [J].
Eiholzer, U ;
Bachmann, S ;
I'Allemand, D .
HORMONE RESEARCH, 2000, 53 :44-52
[9]   Serum ghrelin levels are inversely correlated with body mass index, age, and insulin concentrations in normal children and are markedly increased in Prader-Willi syndrome [J].
Haqq, AM ;
Farooqi, IS ;
O'Rahilly, S ;
Stadler, DD ;
Rosenfeld, RG ;
Pratt, KL ;
LaFranchi, SH ;
Purnell, JQ .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2003, 88 (01) :174-178
[10]  
Ishikawa T, 1996, AM J MED GENET, V62, P350, DOI 10.1002/(SICI)1096-8628(19960424)62:4<350::AID-AJMG6>3.0.CO