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Blunted pancreatic polypeptide responses in children with obesity of Prader-Willi syndrome
Insights
Patients with Prader-Willi syndrome (PWS) show abnormal pancreatic polypeptide (PP) responses to meals, suggesting PP
Area of Science:
- Endocrinology
- Metabolic Disorders
- Neuroscience
Background:
- Obesity is a complex metabolic disorder.
- Prader-Willi syndrome (PWS) is a genetic disorder associated with hyperphagia and obesity.
- Hormonal regulation of appetite is crucial in metabolic health.
Purpose of the Study:
- To investigate the role of pancreatic polypeptide (PP) in appetite regulation.
- To compare hormonal responses to a meal in individuals with PWS, normal weight, and obese controls.
Main Methods:
- Meal stimulation test (275 Kcal) in 10 normal weight, 13 obese, and 7 PWS patients.
- Measurement of serum/plasma concentrations of PP, glucose, insulin, and GIP at 15-minute intervals for 180 minutes.
- Analysis of basal and peak hormonal responses.
Main Results:
- PWS patients exhibited significantly lower glucose responses compared to controls.
- Insulin responses were higher in PWS than normal controls but lower than obese controls.
- Gastric inhibitory polypeptide (GIP) concentrations and peak responses were lower in PWS patients.
- All 7 PWS patients displayed abnormal PP responses, with 5 showing blunted or absent release, suggesting a potential role in appetite control.
Conclusions:
- Blunted pancreatic polypeptide (PP) response in Prader-Willi syndrome (PWS) patients parallels animal models.
- PP may play a significant role in appetite control and the hyperphagia observed in PWS.
- Further research into PP's role in obesity and eating disorders is warranted.
Abstract:
Serum pancreatic polypeptide (PP), gastric inhibitory polypeptide (GIP), insulin and glucose responses to meal stimulation were studied in 10 normal weight patients, 13 normal obese patients and 7 patients with Prader-Willi syndrome (PWS) associated obesity. Serum and plasma concentrations of PP, glucose, insulin and GIP were obtained at 15 min intervals from 0-180 min. after a 275 K calorie meal. Basal and peak responses of glucose, for patients with PWS were significantly lower when compared to normal or obese controls. Basal and peak insulin responses in PWS were significantly greater than those of the normal controls but still less than those of the obese controls. Basal GIP concentrations in the patients with PWS were significantly less than normals and their peak response was less than the obese control group. No significant differences in basal or peak PP responses were noted between normal and obese controls. All 7 patients with PWS had abnormal PP responses. Five failed to show significant PP release after the stimulation; one had a peak response to 130 pg/ml while the 7th patient (PB) had an exaggerated response to 2000 pg/ml. The 6 patients with low or no response had basal PP values of 62 +/- 12 pg/ml and a mean PP peak response of 78 +/- 15 pg/ml. This observation of blunted PP response in a human model of hyperphagia and obesity parallels the animal models and suggests PP may have a significant role in appetite control.