ArticleDiabetes2011
Progressive erosion of β-cell function precedes the onset of hyperglycemia in the NOD mouse model of type 1 diabetes.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 74 citations in OpenAlex.
- Longitudinal monitoring of type 1 diabetes progression to disease onset.Science advances · 2026Article
- Revisiting type 1 diabetes progression in the non-obese diabetic mouse.Scientific reports · 2026Article
- Submicron-sized ultrasound contrast agents as therapeutic peptide delivery vehicles in type 1 diabetes.Theranostics · 2026Article
- Partial remission of type 1 diabetes: Do immunometabolic events define the honeymoon period?Diabetes, obesity & metabolism · 2025Review
- Refined protocol for newly onset identification in non-obese diabetic mice: an animal-friendly, cost-effective, and efficient alternative.Laboratory animal research · 2024Article
- Immunotherapy With Low-Dose IL-2/CD25 Prevents β-Cell Dysfunction and Dysglycemia in Prediabetic NOD Mice.Diabetes · 2023Article
- β-Cell Cre Expression and Reduced Ins1 Gene Dosage Protect Mice From Type 1 Diabetes.Endocrinology · 2022Article
- ICAM-1 Abundance Is Increased in Pancreatic Islets of Hyperglycemic Female NOD Mice and Is Rapidly Upregulated by NF-κB in Pancreatic β-Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Modulation of Gap Junction Coupling Within the Islet of Langerhans During the Development of Type 1 Diabetes.Frontiers in physiology · 2022Article
- Syntaxin 4 Enrichment in β-Cells Prevents Conversion to Autoimmune Diabetes in Non-Obese Diabetic (NOD) Mice.Diabetes · 2021Article
- Expression of Human Mutant Preproinsulins Induced Unfolded Protein Response,International journal of molecular sciences · 2021Article
- Detecting insulitis in type 1 diabetes with ultrasound phase-change contrast agents.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Regulation of Tissue Inflammation by 12-Lipoxygenases.Biomolecules · 2021Review
- Inherent Beta Cell Dysfunction Contributes to Autoimmune Susceptibility.Biomolecules · 2021Review
- Article
- The role of beta-cell dysfunction in early type 1 diabetes.Current opinion in endocrinology, diabetes, and obesity · 2020Review
- TIR-Domain-Containing Adaptor-Inducing Interferon-International journal of endocrinology · 2020Article
- Endoplasmic reticulum stress-induced cellular dysfunction and cell death in insulin-producing cells results in diabetes-like phenotypes inBiology open · 2019Article
- Therapeutic administration of Tregitope-Human Albumin Fusion with Insulin Peptides to promote Antigen-Specific Adaptive Tolerance Induction.Scientific reports · 2019Article
- Inhibition of Cathepsin S Reduces Lacrimal Gland Inflammation and Increases Tear Flow in a Mouse Model of Sjögren's Syndrome.Scientific reports · 2019Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveA progressive decline in insulin responses to glucose was noted in individuals before the onset of type 1 diabetes. We determined whether such abnormalities occurred in prediabetic NOD mice-the prototypic model for human type 1 diabetes. RESEARCH DESIGN AND
methodsMorning blood glucose was measured every other day in a cohort of NOD females. Glucose tolerance and insulin secretion were measured longitudinally by intraperitoneal glucose tolerance tests in NOD/ShiLtJ and BALB/cJ mice 6 to 14 weeks of age. Arginine-stimulated insulin secretion and insulin sensitivity were assessed during intraperitoneal arginine or intraperitoneal insulin tolerance tests.
resultsDuring prediabetes, NOD females displayed a progressive increase in glucose levels followed by an acute onset of hyperglycemia. First-phase insulin responses (FPIRs) during the intraperitoneal glucose tolerance test (IPGTT) declined before loss of glucose tolerance in NOD. The failure of FPIR could be detected, with a decline in peak insulin secretion during IPGTT. Arginine-stimulated insulin secretion remained unchanged during the study period. The decline in insulin secretion in NOD mice could not be explained by changes in insulin sensitivity.
conclusionsThere was an impressive decline in FPIR before changes in glucose tolerance, suggesting that impairment of FPIR is an early in vivo marker of progressive β-cell failure in NOD mice and human type 1 diabetes. We portend that these phenotypes in NOD mice follow a similar pattern to those seen in humans with type 1 diabetes and validate, in a novel way, the importance of this animal model for studies of this disease.
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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.