Snord116 is critical in the regulation of food intake and body weight

• DOI: 10.1038/srep18614
• Publication Date: 2016-01-04T09:58:53Z
• Authors: Yue Qi; Louise Purtell; Melissa Fu; Nicola J. Lee; Julia Aepler; Lei Zhang; Kim Loh; Ronaldo F. Enriquez; Paul A. Baldock; Sergei Zolotukhin; Lesley V. Campbell; Herbert Herzog
• Keywords: Male; 0301 basic medicine; Biomedical and clinical sciences; 5202 Biological Psychology; Gene Expression; 32 Biomedical and Clinical Sciences; Mice; Eating; Endocrinology; 2.1 Biological and endogenous factors; Pediatric; Mice, Knockout; Neurons; 2. Zero hunger; 3. Good health; Multidisciplinary Sciences; 52 Psychology; Body Composition; Science & Technology - Other Topics; Carbohydrate Metabolism; Female; anzsrc-for: 5202 Biological Psychology; 570; Knockout; Hypothalamus; Diet, High-Fat; Article; anzsrc-for: 52 Psychology; 03 medical and health sciences; anzsrc-for: 32 Biomedical and Clinical Sciences; Genetics; Animals; RNA, Small Nucleolar; Obesity; Metabolic and endocrine; Nutrition; Small Nucleolar; Science & Technology; Appetite Regulation; Body Weight; Neuropeptides; Neurosciences; ENERGY-EXPENDITURE; Diet; High-Fat; Medical genetics (excl. cancer genetics); RNA; PRADER-WILLI-SYNDROME; Energy Metabolism

Abstract Prader-Willi syndrome (PWS) is the predominant genetic cause of obesity in humans. Recent clinical reports have suggested that micro-deletion Snord116 gene cluster can lead to PWS, however, extent contributions encoded snoRNAs unknown. Here we show mice lacking globally low birth weight, increased body weight gain, energy expenditure and hyperphagia. Consistent with this, microarray analysis hypothalamic expression revealed a significant alteration feeding related pathways was also confirmed by situ hybridisation. Importantly, selective deletion only from NPY expressing neurons mimics almost exactly global phenotype including persistent gain early adulthood, Mechanistically, lack leads upregulation mRNA consistent hyperphagic suggests critical role control neuronal functions might be dysregulated PWS.