Ghrelin levels in young children with Prader-Willi syndrome

被引:41
作者
Erdie-Lalena, Christine R.
Holm, Vanja A.
Kelly, Patrick C.
Frayo, R. Scott
Cummings, David E.
机构
[1] Univ Washington, VA Puget Sound Hlth Care Syst, SIII Endo, Dept Med,Div Metab Endocrinol & Nutr, Seattle, WA 98108 USA
[2] Madigan Army Med Ctr, Dept Pediat, Div Dev & Behav Pediat, Ft Lewis, WA USA
[3] Univ Washington, Sch Med, Ctr Human Dev & Disabil, Dept Pediat, Seattle, WA 98195 USA
关键词
D O I
10.1016/j.jpeds.2006.04.011
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Objective To explore the hypothesis that high ghrelin levels contribute to obesity in Prader-Willi syndrome (PWS), we assessed whether the increased levels observed in older persons with PWS exist in very young children, before the onset of hyperphagia. Study design We measured ghrelin levels in nine children with PWS (17-60 months of age) and eight healthy control subjects of equivalent body mass index (BMI), age, and sex. Results PWS and control groups had equivalent BMI (16.8 +/- 1.4 vs 16.1 +/- 0.9 kg/m(2), respectively; P = .24), age (37.8 +/- 15.4 vs 50.3 +/- 17.7 months; P = .14), and sex. PWS and control groups also had equivalent fasting levels of total ghrelin (787 242 vs 716 135 pg/mL, respectively; P = .24), bioactive ghrelin (102 +/- 35 vs 91 +/- 23 pg/mL; P = .45), insulin, and glucose. Ghrelin correlated negatively with BMI among controls (r = -0.760, P = .029) but not PWS (r = 0.015, P = .97). Conclusions Children < 5 years of age with PWS, who had not yet developed hyperphagia or excessive obesity, had normal ghrelin levels, in contrast with the hyperghrelinemia of older, hyperphagic people with PWS. It is possible that ghrelin levels increase suddenly before hyperphagia develops.
引用
收藏
页码:199 / 204
页数:6
相关论文
共 56 条
[1]   Delayed short-term secretory regulation of ghrelin in obese animals: Evidenced by a specific RIA for the active form of ghrelin [J].
Ariyasu, H ;
Takaya, K ;
Hosoda, H ;
Iwakura, H ;
Ebihara, K ;
Mori, K ;
Ogawa, Y ;
Hosoda, K ;
Akamizu, T ;
Kojima, M ;
Kangawa, K ;
Nakao, K .
ENDOCRINOLOGY, 2002, 143 (09) :3341-3350
[2]   Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin [J].
Asakawa, A ;
Inui, A ;
Kaga, T ;
Yuzuriha, H ;
Nagata, T ;
Ueno, N ;
Makino, S ;
Fujimiya, M ;
Niijima, A ;
Fujino, MA ;
Kasuga, M .
GASTROENTEROLOGY, 2001, 120 (02) :337-345
[3]   Antagonism of ghrelin receptor reduces food intake and body weight gain in mice [J].
Asakawa, A ;
Inui, A ;
Kaga, T ;
Katsuura, G ;
Fujimiya, M ;
Fujino, MA ;
Kasuga, M .
GUT, 2003, 52 (07) :947-952
[4]   Endogenous ghrelin is an orexigenic peptide acting in the arcuate nucleus in response to fasting [J].
Bagnasco, M ;
Tulipano, G ;
Melis, MR ;
Argiolas, A ;
Cocchi, D ;
Muller, EE .
REGULATORY PEPTIDES, 2003, 111 (1-3) :161-167
[5]   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
[6]   Ghrelin and reproduction: a novel signal linking energy status and fertility? [J].
Barreiro, ML ;
Tena-Sempere, M .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2004, 226 (1-2) :1-9
[7]   Prevalence of, and risk factors for, physical ill-health in people with Prader-Willi syndrome: a population-based study [J].
Butler, JV ;
Whittington, JE ;
Holland, AJ ;
Boer, H ;
Clarke, D ;
Webb, T .
DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY, 2002, 44 (04) :248-255
[8]  
Butler MG, 2004, J PEDIATR ENDOCR MET, V17, P1177
[9]   Behavioral differences among subjects with Prader-Willi syndrome and type I or type II deletion and maternal disomy [J].
Butler, MG ;
Bittel, DC ;
Kibiryeva, N ;
Talebizadeh, Z ;
Thompson, T .
PEDIATRICS, 2004, 113 (03) :565-573
[10]  
Cassidy S.B., 2005, MANAGEMENT GENETIC S, P429