Abstract
ContextPrader-Willi syndrome (PWS) is characterized by severe hyperphagia. Brain-derived neurotrophic factor (BDNF) and leptin are reciprocally involved in energy homeostasis.ObjectivesTo analyze the role of BDNF and leptin in satiety in genetic subtypes of PWS.DesignExperimental study.SettingUniversity hospital.Subjects90 adults: 30 PWS patients; 30 age-sex-BMI-matched obese controls; and 30 age-sex-matched lean controls.InterventionsSubjects ingested a liquid meal after fasting ≥10 hours.Main Outcome MeasuresLeptin and BDNF levels in plasma extracted before ingestion and 30’, 60’, and 120’ after ingestion. Hunger, measured on a 100-point visual analogue scale before ingestion and 60’ and 120’ after ingestion.ResultsFasting BDNF levels were lower in PWS than in controls (p = 0.05). Postprandially, PWS patients showed only a truncated early peak in BDNF, and their BDNF levels at 60' and 120' were lower compared with lean controls (p<0.05). Leptin was higher in PWS patients than in controls at all time points (p<0.001). PWS patients were hungrier than controls before and after eating. The probability of being hungry was associated with baseline BDNF levels: every 50-unit increment in BDNF decreased the odds of being hungry by 22% (OR: 0.78, 95%CI: 0.65–0.94). In uniparental disomy, the odds of being hungry decreased by 66% (OR: 0.34, 90%CI: 0.13–0.9). Postprandial leptin patterns did no differ among genetic subtypes.ConclusionsLow baseline BDNF levels and lack of postprandial peak may contribute to persistent hunger after meals. Uniparental disomy is the genetic subtype of PWS least affected by these factors.
Highlights
Prader-Willi syndrome (PWS) is a genetic disorder caused by the lack of expression of the paternally inherited genetic material located at 15q11-q13
The probability of being hungry was associated with baseline Brain-derived neurotrophic factor (BDNF) levels: every 50-unit increment in BDNF decreased the odds of being hungry by 22% (OR: 0.78, 95%CI: 0.65–0.94)
The odds of being hungry decreased by 66% (OR: 0.34, 90%CI: 0.13–0.9)
Summary
Prader-Willi syndrome (PWS) is a genetic disorder caused by the lack of expression of the paternally inherited genetic material located at 15q11-q13. This lack of expression is due to a deletion (subtype I or II) of a region of the paternally inherited chromosome 15 in 65% to 75% of cases, to maternal uniparental disomy (UPD) in 20% to 30% (both copies of chromosome 15 are inherited from the mother), or to an imprinting defect in 1% to 3% [1]. Other molecules that could explain the lack of satiety in PWS have been sought, to date, our understanding of this problem remains poor due to the complexity of the hunger-satiety circuitry
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