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Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome.
Int J Obes (Lond) 2012; 36(12):1564-70IJ

Abstract

OBJECTIVE

Prader-Willi syndrome (PWS) is a genetic neurodevelopmental disorder with several nutritional phases during childhood proceeding from poor feeding, through normal eating without and with obesity, to hyperphagia and life-threatening obesity, with variable ages of onset. We investigated whether differences in appetite hormones may explain the development of abnormal eating behaviour in young children with PWS.

SUBJECTS

In this cross-sectional study, children with PWS (n=42) and controls (n=9) aged 7 months-5 years were recruited. Mothers were interviewed regarding eating behaviour, and body mass index (BMI) was calculated. Fasting plasma samples were assayed for insulin, leptin, glucose, peptide YY (PYY), ghrelin and pancreatic polypeptide (PP).

RESULTS

There was no significant relationship between eating behaviour in PWS subjects and the levels of any hormones or insulin resistance, independent of age. Fasting plasma leptin levels were significantly higher (mean ± s.d.: 22.6 ± 12.5 vs 1.97 ± 0.79 ng ml(-1), P=0.005), and PP levels were significantly lower (22.6 ± 12.5 vs 69.8 ± 43.8 pmol l(-1), P<0.001) in the PWS group compared with the controls, and this was independent of age, BMI, insulin resistance or IGF-1 levels. However, there was no significant difference in plasma insulin, insulin resistance or ghrelin levels between groups, though PYY declined more rapidly with age but not BMI in PWS subjects.

CONCLUSION

Even under the age of 5 years, PWS is associated with low levels of anorexigenic PP, as in older children and adults. Hyperghrelinaemia or hypoinsulinaemia was not seen in these young children with PWS. Change in these appetite hormones was not associated with the timing of the transition to the characteristic hyperphagic phase. However, abnormal and/or delayed development or sensitivity of the effector pathways of these appetitive hormones (for example, parasympathetic and central nervous system) may interact with low PP levels, and later hyperghrelinaemia or hypoinsulinaemia, to contribute to hyperphagia in PWS.

Authors+Show Affiliations

Metabolic and Molecular Imaging Group, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, UK. tony.goldstone@imperial.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22270375

Citation

Goldstone, A P., et al. "Appetite Hormones and the Transition to Hyperphagia in Children With Prader-Willi Syndrome." International Journal of Obesity (2005), vol. 36, no. 12, 2012, pp. 1564-70.
Goldstone AP, Holland AJ, Butler JV, et al. Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome. Int J Obes (Lond). 2012;36(12):1564-70.
Goldstone, A. P., Holland, A. J., Butler, J. V., & Whittington, J. E. (2012). Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome. International Journal of Obesity (2005), 36(12), pp. 1564-70. doi:10.1038/ijo.2011.274.
Goldstone AP, et al. Appetite Hormones and the Transition to Hyperphagia in Children With Prader-Willi Syndrome. Int J Obes (Lond). 2012;36(12):1564-70. PubMed PMID: 22270375.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome. AU - Goldstone,A P, AU - Holland,A J, AU - Butler,J V, AU - Whittington,J E, Y1 - 2012/01/24/ PY - 2012/1/25/entrez PY - 2012/1/25/pubmed PY - 2013/5/17/medline SP - 1564 EP - 70 JF - International journal of obesity (2005) JO - Int J Obes (Lond) VL - 36 IS - 12 N2 - OBJECTIVE: Prader-Willi syndrome (PWS) is a genetic neurodevelopmental disorder with several nutritional phases during childhood proceeding from poor feeding, through normal eating without and with obesity, to hyperphagia and life-threatening obesity, with variable ages of onset. We investigated whether differences in appetite hormones may explain the development of abnormal eating behaviour in young children with PWS. SUBJECTS: In this cross-sectional study, children with PWS (n=42) and controls (n=9) aged 7 months-5 years were recruited. Mothers were interviewed regarding eating behaviour, and body mass index (BMI) was calculated. Fasting plasma samples were assayed for insulin, leptin, glucose, peptide YY (PYY), ghrelin and pancreatic polypeptide (PP). RESULTS: There was no significant relationship between eating behaviour in PWS subjects and the levels of any hormones or insulin resistance, independent of age. Fasting plasma leptin levels were significantly higher (mean ± s.d.: 22.6 ± 12.5 vs 1.97 ± 0.79 ng ml(-1), P=0.005), and PP levels were significantly lower (22.6 ± 12.5 vs 69.8 ± 43.8 pmol l(-1), P<0.001) in the PWS group compared with the controls, and this was independent of age, BMI, insulin resistance or IGF-1 levels. However, there was no significant difference in plasma insulin, insulin resistance or ghrelin levels between groups, though PYY declined more rapidly with age but not BMI in PWS subjects. CONCLUSION: Even under the age of 5 years, PWS is associated with low levels of anorexigenic PP, as in older children and adults. Hyperghrelinaemia or hypoinsulinaemia was not seen in these young children with PWS. Change in these appetite hormones was not associated with the timing of the transition to the characteristic hyperphagic phase. However, abnormal and/or delayed development or sensitivity of the effector pathways of these appetitive hormones (for example, parasympathetic and central nervous system) may interact with low PP levels, and later hyperghrelinaemia or hypoinsulinaemia, to contribute to hyperphagia in PWS. SN - 1476-5497 UR - https://www.unboundmedicine.com/medline/citation/22270375/Appetite_hormones_and_the_transition_to_hyperphagia_in_children_with_Prader_Willi_syndrome_ L2 - http://dx.doi.org/10.1038/ijo.2011.274 DB - PRIME DP - Unbound Medicine ER -