ArticleDiabetologia2013
Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.
Article in Diabetologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Emerging Role of Transcription Factor 19 (TCF19) in Inflammatory Disease and Cancer.Biomolecules · 2026Review
- A bioinformatics screen identifies TCF19 as an aggressiveness-sustaining gene in prostate cancer.Molecular oncology · 2025Article
- TCF19 Impacts a Network of Inflammatory and DNA Damage Response Genes in the Pancreatic β-Cell.Metabolites · 2021Article
- Postnatal maturation of calcium signaling in islets of Langerhans from neonatal mice.Cell calcium · 2021Article
- NUPR1 preserves insulin secretion of pancreatic β-cells during inflammatory stress by multiple low-dose streptozotocin and high-fat diet.American journal of physiology. Endocrinology and metabolism · 2020Article
- p8 deficiency leads to elevated pancreatic beta cell mass but does not contribute to insulin resistance in mice fed with high-fat diet.PloS one · 2018Article
- A liver stress-endocrine nexus promotes metabolic integrity during dietary protein dilution.The Journal of clinical investigation · 2016Article
- Nutritional systems biology of type 2 diabetes.Genes & nutrition · 2015Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
aims/hypothesisThe stress-activated nuclear protein transcription regulator 1 (NUPR1) is induced in response to glucose and TNF-α, both of which are elevated in type 2 diabetes, and Nupr1 has been implicated in cell proliferation and apoptosis cascades. We used Nupr1(-/-) mice to study the role of Nupr1 in glucose homeostasis under normal conditions and following maintenance on a high-fat diet (HFD).
methodsGlucose homeostasis in vivo was determined by measuring glucose tolerance, insulin sensitivity and insulin secretion. Islet number, morphology and beta cell area were assessed by immunofluorescence and morphometric analysis, and islet cell proliferation was quantified by analysis of BrdU incorporation. Islet gene expression was measured by gene arrays and quantitative RT-PCR, and gene promoter activities were monitored by measuring luciferase activity.
resultsNupr1(-/-) mice had increased beta cell mass as a consequence of enhanced islet cell proliferation. Nupr1-dependent suppression of beta cell Ccna2 and Tcf19 promoter activities was identified as a mechanism through which Nupr1 may regulate beta cell cycle progression. Nupr1(-/-) mice maintained on a normal diet were mildly insulin resistant, but were normoglycaemic with normal glucose tolerance because of compensatory increases in basal and glucose-induced insulin secretion. Nupr1 deletion was protective against HFD-induced obesity, insulin resistance and glucose intolerance. CONCLUSIONS/
interpretationInhibition of NUPR1 expression or activity has the potential to protect against the metabolic defects associated with obesity and type 2 diabetes.
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