PANCREATIC-POLYPEPTIDE INFUSIONS REDUCE FOOD-INTAKE IN PRADER-WILLI SYNDROME

被引:105
作者
BERNTSON, GG
ZIPF, WB
ODORISIO, TM
HOFFMAN, JA
CHANCE, RE
机构
[1] OHIO STATE UNIV,DEPT PSYCHOL,COLUMBUS,OH 43210
[2] OHIO STATE UNIV,DEPT PEDIAT,COLUMBUS,OH 43210
[3] CHILDRENS HOSP,COLUMBUS,OH 43205
[4] ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285
关键词
PANCREATIC POLYPEPTIDE; PRADER-WILLI SYNDROME; FOOD INTAKE; HUNGER; SATIETY;
D O I
10.1016/0196-9781(93)90138-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Prader-Willi syndrome is characterized by dramatic hyperphagia and morbid obesity, and is associated with a deficiency in basal and meal-stimulated serum pancreatic polypeptide (PP) levels. Intravenous infusions of pancreatic polypeptide (90 min, 50 pmol/kg/h) restored normal serum PP levels, and a regimen of morning and afternoon PP infusions was found to significantly reduce food intake in Prader-Willi subjects. Food intake was evaluated in a 60-min free-feeding test that shows high reliability and validity. Basal food intake during saline infusions was striking (almost-equal-to 60 chicken sandwich quarters), and this intake was reduced overall by almost-equal-to 12% during PP infusions. This reduction was apparent only for female subjects, and may have reflected enhanced satiation rather than an overall suppression of food intake. No differences were apparent across subjects, in either basal food intake or the PP-related decrease in food intake, in the presence or absence of the widely recognized chromosomal marker for this syndrome [deletion of 15(q11-q13)]. More specific gene defects as recently reported in these subjects, however, suggest that the Prader-Willi syndrome may represent an important model for the study of food intake regulation.
引用
收藏
页码:497 / 503
页数:7
相关论文
共 53 条
[21]   L-364,718, A NEW CCK ANTAGONIST, INHIBITS POSTPRANDIAL PANCREATIC-SECRETION AND PP RELEASE IN DOGS [J].
HOSOTANI, R ;
CHOWDHURY, P ;
RAYFORD, PL .
DIGESTIVE DISEASES AND SCIENCES, 1989, 34 (03) :462-467
[22]   MECHANISM OF ACTIONS OF CHOLECYSTOKININ OCTAPEPTIDE ON FOOD-INTAKE AND INSULIN AND PANCREATIC-POLYPEPTIDE RELEASE IN THE DOG [J].
INUI, A ;
OKITA, M ;
INOUE, T ;
SAKATANI, N ;
OYA, M ;
MORIOKA, H ;
OGAWA, T ;
MIZUNO, N ;
BABA, S .
PEPTIDES, 1988, 9 (05) :1093-1100
[23]  
JIA BQ, 1984, GASTROENTEROLOGY, V87, P338
[24]  
JORDE R, 1984, INT J OBESITY, V8, P393
[25]   CCK RECEPTORS IN RELEASE OF PANCREATIC-POLYPEPTIDE (PP) IN DOGS [J].
KONTUREK, SJ ;
KONTUREK, P ;
BIELANSKI, W ;
SZEWCZYK, K .
DIGESTIVE DISEASES AND SCIENCES, 1989, 34 (06) :849-856
[26]  
LARSON GM, 1985, SURGERY, V98, P236
[27]  
LEDBETTER DH, 1982, AM J HUM GENET, V34, P278
[28]   REGULATION OF PANCREATIC ENDOCRINE FUNCTION BY CHOLECYSTOKININ - STUDIES WITH MK-329, A NONPEPTIDE CHOLECYSTOKININ RECEPTOR ANTAGONIST [J].
LIDDLE, RA ;
GERTZ, BJ ;
KANAYAMA, S ;
BECCARIA, L ;
GETTYS, TW ;
TAYLOR, IL ;
RUSHAKOFF, RJ ;
WILLIAMS, VC ;
COKER, LD .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1990, 70 (05) :1312-1318
[29]  
Lin T., 1978, GUT HORM, P242
[30]   PANCREATIC POLYPEPTIDE - POSSIBLE ROLE IN REGULATION OF FOOD-INTAKE IN MOUSE - HYPOTHESIS [J].
MALAISSELAGAE, F ;
CARPENTIER, JL ;
PATEL, YC ;
MALAISSE, WJ ;
ORCI, L .
EXPERIENTIA, 1977, 33 (07) :915-917