ArticleThe Journal of clinical investigation2018
Neuronatin regulates pancreatic β cell insulin content and secretion.
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 33 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.
The trial behind it
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
33 citing papers in PubMed, 64 citations in OpenAlex.
- Resolving thyroid lineage cell trajectories merging into a dual endocrine gland in mammals.Nature communications · 2026Article
- Genome-wide cell type-specific and sex-specific transcriptional dysregulation in the islet of Langerhans underlies islet dysfunction in Down syndrome-related diabetes.bioRxiv : the preprint server for biology · 2026Article
- Neuronatin Influences Endothelial Homeostasis and Atherosclerosis via ER-Mitochondria Interactions.Journal of inflammation research · 2026Article
- Microproteins in Metabolic Biology: Emerging Functions and Potential Roles as Nutrient-Linked Biomarkers.International journal of molecular sciences · 2025Review
- Unraveling molecular signatures and prognostic biomarkers in glioblastoma: a comprehensive study on treatment resistance and personalized strategies.Discover oncology · 2024Article
- PARN Maintains RNA Stability to Regulate Insulin Maturation and GSIS in Pancreatic β Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Exploring pancreatic beta-cell subgroups and their connectivity.Nature metabolism · 2024Review
- Developmentally dynamic changes in DNA methylation in the human pancreas.BMC genomics · 2024Article
- Differential CpG methylation at Nnat in the early establishment of beta cell heterogeneity.Diabetologia · 2024Article
- The MODY-associatedeLife · 2024Article
- Differential CpG methylation atbioRxiv : the preprint server for biology · 2023Article
- NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development.Nature communications · 2023Article
- Circulating Neuronatin Levels Are Positively Associated with BMI and Body Fat Mass but Not with Psychological Parameters.Nutrients · 2023Article
- Adversarial training improves model interpretability in single-cell RNA-seq analysis.Bioinformatics advances · 2023Article
- Independent phenotypic plasticity axes define distinct obesity sub-types.Nature metabolism · 2022Article
- Article
- Transcriptional atlas analysis from multiple tissues reveals the expression specificity patterns in beef cattle.BMC biology · 2022Article
- β-synuclein potentiates synaptic vesicle dopamine uptake and rescues dopaminergic neurons from MPTP-induced death in the absence of other synucleins.The Journal of biological chemistry · 2021Article
- Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity.Scientific reports · 2021Article
- Sexually dimorphic roles for the type 2 diabetes-associated C2cd4b gene in murine glucose homeostasis.Diabetologia · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 9 institutions in 4 countries.
Funding
Abstract
Neuronatin (Nnat) is an imprinted gene implicated in human obesity and widely expressed in neuroendocrine and metabolic tissues in a hormone- and nutrient-sensitive manner. However, its molecular and cellular functions and precise role in organismal physiology remain only partly defined. Here we demonstrate that mice lacking Nnat globally or specifically in β cells display impaired glucose-stimulated insulin secretion leading to defective glucose handling under conditions of nutrient excess. In contrast, we report no evidence for any feeding or body weight phenotypes in global Nnat-null mice. At the molecular level neuronatin augments insulin signal peptide cleavage by binding to the signal peptidase complex and facilitates translocation of the nascent preprohormone. Loss of neuronatin expression in β cells therefore reduces insulin content and blunts glucose-stimulated insulin secretion. Nnat expression, in turn, is glucose-regulated. This mechanism therefore represents a novel site of nutrient-sensitive control of β cell function and whole-animal glucose homeostasis. These data also suggest a potential wider role for Nnat in the regulation of metabolism through the modulation of peptide processing events.
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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.