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Snord116 is critical in the regulation of food intake and body weight
- Source :
- Scientific Reports
- Publication Year :
- 2015
-
Abstract
- Prader-Willi syndrome (PWS) is the predominant genetic cause of obesity in humans. Recent clinical reports have suggested that micro-deletion of the Snord116 gene cluster can lead to PWS, however, the extent of the contributions of the encoded snoRNAs is unknown. Here we show that mice lacking Snord116 globally have low birth weight, increased body weight gain, energy expenditure and hyperphagia. Consistent with this, microarray analysis of hypothalamic gene expression revealed a significant alteration in feeding related pathways that was also confirmed by in situ hybridisation. Importantly, selective deletion of Snord116 only from NPY expressing neurons mimics almost exactly the global deletion phenotype including the persistent low birth weight, increased body weight gain in early adulthood, increased energy expenditure and hyperphagia. Mechanistically, the lack of Snord116 in NPY neurons leads to the upregulation of NPY mRNA consistent with the hyperphagic phenotype and suggests a critical role of Snord116 in the control of NPY neuronal functions that might be dysregulated in PWS.
- Subjects :
- 0301 basic medicine
Male
medicine.medical_specialty
Hypothalamus
Neuropeptide
Gene Expression
Diet, High-Fat
Article
03 medical and health sciences
Eating
0302 clinical medicine
Downregulation and upregulation
Internal medicine
Gene expression
medicine
Animals
RNA, Small Nucleolar
Obesity
Mice, Knockout
Neurons
Multidisciplinary
Microarray analysis techniques
business.industry
Appetite Regulation
Body Weight
Neuropeptides
nutritional and metabolic diseases
medicine.disease
Phenotype
Low birth weight
030104 developmental biology
Endocrinology
Body Composition
Carbohydrate Metabolism
Female
medicine.symptom
business
Energy Metabolism
030217 neurology & neurosurgery
Subjects
Details
- ISSN :
- 20452322
- Volume :
- 6
- Database :
- OpenAIRE
- Journal :
- Scientific reports
- Accession number :
- edsair.doi.dedup.....edd49c863cd0a922e3f745f6c5945cb9