ArticleMolecular metabolism2018
Neuronatin deletion causes postnatal growth restriction and adult obesity in 129S2/Sv mice.
Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Genetics of Anorexia Nervosa: Translation to Future Personalized Therapies.The Psychiatric clinics of North America · 2025Review
- Father's adolescent body silhouette is associated with offspring asthma, lung function and BMI through DNA methylation.Communications biology · 2025Article
- Differential CpG methylation at Nnat in the early establishment of beta cell heterogeneity.Diabetologia · 2024Article
- Differential CpG methylation atbioRxiv : the preprint server for biology · 2023Article
- Promoting metabolic inefficiency for metabolic disease.iScience · 2023Review
- Circulating Neuronatin Levels Are Positively Associated with BMI and Body Fat Mass but Not with Psychological Parameters.Nutrients · 2023Article
- Identification of adipose tissue transcriptomic memory of anorexia nervosa.Molecular medicine (Cambridge, Mass.) · 2023Article
- In silico identification of the rare-coding pathogenic mutations and structural modeling of human NNAT gene associated with anorexia nervosa.Eating and weight disorders : EWD · 2022Article
- Independent phenotypic plasticity axes define distinct obesity sub-types.Nature metabolism · 2022Article
- Black Tea Reduces Diet-Induced Obesity in Mice via Modulation of Gut Microbiota and Gene Expression in Host Tissues.Nutrients · 2022Article
- Paternal dietary ratio of n-6: n-3 polyunsaturated fatty acids programs offspring leptin expression and gene imprinting in mice.Frontiers in nutrition · 2022Article
- The effects of neurogranin knockdown on SERCA pump efficiency in soleus muscles of female mice fed a high fat diet.Frontiers in endocrinology · 2022Article
- The Evolutionary Advantage in Mammals of the Complementary Monoallelic Expression Mechanism of Genomic Imprinting and Its Emergence From a Defense Against the Insertion Into the Host Genome.Frontiers in genetics · 2022Review
- Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity.Scientific reports · 2021Article
- Neuronatin regulates whole-body metabolism: is thermogenesis involved?FASEB bioAdvances · 2020Article
- Genomic imprinting and its effects on postnatal growth and adult metabolism.Cellular and molecular life sciences : CMLS · 2019Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveImprinted genes are crucial for the growth and development of fetal and juvenile mammals. Altered imprinted gene dosage causes a variety of human disorders, with growth and development during these crucial early stages strongly linked with future metabolic health in adulthood. Neuronatin (Nnat) is a paternally expressed imprinted gene found in neuroendocrine systems and white adipose tissue and is regulated by the diet and leptin. Neuronatin expression is downregulated in obese children and has been associated with stochastic obesity in C57BL/6 mice. However, our recent studies of Nnat null mice on this genetic background failed to display any body weight or feeding phenotypes but revealed a defect in glucose-stimulated insulin secretion due to the ability of neuronatin to potentiate signal peptidase cleavage of preproinsulin. Nnat deficiency in beta cells therefore caused a lack of appropriate storage and secretion of mature insulin.
methodsTo further explore the potential role of Nnat in the regulation of body weight and adiposity, we studied classical imprinting-related phenotypes such as placental, fetal, and postnatal growth trajectory patterns that may impact upon subsequent adult metabolic phenotypes.
resultsHere we find that, in contrast to the lack of any body weight or feeding phenotypes on the C57BL/6J background, deletion of Nnat in mice on 129S2/Sv background causes a postnatal growth restriction with reduced adipose tissue accumulation, followed by catch up growth after weaning. This was in the absence of any effect on fetal growth or placental development. In adult 129S2/Sv mice, Nnat deletion was associated with hyperphagia, reduced energy expenditure, and partial leptin resistance. Lack of neuronatin also potentiated obesity caused by either aging or high fat diet feeding.
conclusionsThe imprinted gene Nnat plays a key role in postnatal growth, adult energy homeostasis, and the pathogenesis of obesity via catch up growth effects, but this role is dependent upon genetic background.
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