{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cimino I"],"funding":["the Medical Research Council","British Heart Foundation","BHF programme grant","Metabolic Disease Unit","Medical Research Council","National Institute for Health Research (NIHR)","Wellcome Trust"],"pagination":["17571"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8413370"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["Neuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat<sup>+/-p</sup> mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat<sup>+/-p</sup> mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry"],"journal":["Scientific reports"],"pubmed_title":["Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity."],"pmcid":["PMC8413370"],"funding_grant_id":["MC_UU_00014/1","NF-SI-0616-10065","RG/12/13/29853","220271/Z/20/Z","RG_18_7_33636","MRC_MC_UU_00014/5","G0400192","MC_UU_12012/5","MC_UU_12012/3","G0802051","MC_UU_12012/2","MC_UU_12012/1","MC_UU_12012/5/B","207462/Z/17/Z","RG/18/7/33636","MC_UU_00014/5","MC_G0802535","MC_UU_00014/3","208363/Z/17/Z","MC_UU_00014/2","100574/Z/12/Z"],"pubmed_authors":["Gribble FM","Larraufie P","Vidal-Puig A","Lawler K","Lam BYH","Ma MKL","Reimann F","Saudek V","Virtue S","Pospisilik JA","Coll AP","Tung YCL","Yeo GSH","Rimmington D","Zvetkova I","Cimino I","Fagnocchi L","Farooqi IS","Kay RG","O'Rahilly S"],"additional_accession":[]},"is_claimable":false,"name":"Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity.","description":"Neuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat<sup>+/-p</sup> mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat<sup>+/-p</sup> mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2026-05-08T10:09:45.229Z","creation":"2022-02-11T10:17:35.525Z"},"accession":"S-EPMC8413370","cross_references":{"pubmed":["34475432"],"doi":["10.1038/s41598-021-96278-8"]}}