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Review
. 2016 Aug;63(1):47-77.
doi: 10.1016/j.yapd.2016.04.005.

Prader Willi Syndrome: Genetics, Metabolomics, Hormonal Function, and New Approaches to Therapy

Krystal A Irizarry  1 , Mark Miller  1 , Michael Freemark  1 , Andrea M Haqq  2
Affiliations
Review

Prader Willi Syndrome: Genetics, Metabolomics, Hormonal Function, and New Approaches to Therapy

Krystal A Irizarry et al. Adv Pediatr. 2016 Aug.
No abstract available

Keywords: Childhood obesity syndrome; Growth hormone; Hyperphagia; Imprinting defect.

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Figures

Figure 1
Figure 1
Representation of chromosome 15q11-13
Figure 2
Figure 2
Physical Findings in PWS
Figure 3
Figure 3
Algorithm for Initiation of GH Therapy in Infants and Children
Figure 4
Figure 4
Timeline of nutritional phases in PWS (adapted from Miller J, et al. 2011 Am J Med Genet Part A 155:1040–1049).
See this image and copyright information in PMC

References

    1. Cassidy SB, Dykens E, Williams CA. Prader-Willi and Angelman syndromes: Sister imprinted disorders. American Journal of Medical Genetics. 2000;97(2):136–146. - PubMed
    1. Bervini S, Herzog H. Mouse models of Prader–Willi Syndrome: A systematic review. Front Neuroendocrinol. 2013;34(2):107–119. - PubMed
    1. Miller NLG, Wevrick R, Mellon PL. Necdin, a Prader–Willi syndrome candidate gene, regulates gonadotropin-releasing hormone neurons during development. Hum Mol Genet. 2009;18(2):248–260. - PMC - PubMed
    1. Bischof JM, Stewart CL, Wevrick R. Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi syndrome. Hum Mol Genet. 2007;16(22):2713–2719. - PubMed
    1. Ding F, Li HH, Zhang S, et al. SnoRNA Snord116 Deletion Causes Growth Deficiency and Hyperphagia in Mice. PLoS ONE. 2008;3(3):e1709. - PMC - PubMed

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