ArticleThe Journal of clinical investigation2018
Hypothalamic loss of Snord116 and Prader-Willi syndrome hyperphagia: the buck stops here?
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Effects of thermoneutrality on food intake, body weight, and body composition in a Prader-Willi syndrome mouse model.Obesity (Silver Spring, Md.) · 2023Article
- Next Steps in Prader-Willi Syndrome Research: On the Relationship between Genotype and Phenotype.International journal of molecular sciences · 2022Review
- Advances in the Development of Nonpeptide Small Molecules Targeting Ghrelin Receptor.Journal of medicinal chemistry · 2022Review
- "A LEAP 2 conclusions? Targeting the ghrelin system to treat obesity and diabetes".Molecular metabolism · 2021Review
- What can we learn from PWS and SNORD116 genes about the pathophysiology of addictive disorders?Molecular psychiatry · 2021Review
- Functional diversity of small nucleolar RNAs.Nucleic acids research · 2020Article
- Ghrelin Receptor Agonist Rescues Excess Neonatal Mortality in a Prader-Willi Syndrome Mouse Model.Endocrinology · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Hyperphagia and obesity are the best-known manifestations of Prader-Willi syndrome (PWS) and are responsible for most of the overall morbidity and mortality associated with the disease. Yet these PWS symptoms remain poorly understood and without effective pharmacologic therapies. Mouse models attempting to recapitulate both the genetic alterations and marked hyperphagia plus obesity of PWS have been enigmatic, leading to skepticism about the use of mouse models to investigate PWS. In this issue of the JCI, Polex-Wolf and colleagues challenge the skeptics by successfully inducing hyperphagia following bilateral mediobasal hypothalamic deletion of the Snord116 gene from adult mice. Obesity also resulted, although only in a subset of mice. While this approach represents an exciting advance, highlighting a pathologic effect of loss of mediobasal hypothalamic Snord116 expression on the development of PWS's hallmark symptoms, the variability in the body-weight and body composition responses to this site-selective gene deletion raises several questions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.