ArticleClinical and experimental immunology2011
2α-Methyl-19-nor-(20S)-1,25-dihydroxyvitamin D(3) protects the insulin 2 knockout non-obese diabetic mouse from developing type 1 diabetes without hypercalcaemia.
Article in Clinical and experimental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.
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Who cites it
5 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The role of vitamin D signalling in β cell apoptosis: a systematic review.Apoptosis : an international journal on programmed cell death · 2026Pooled it
- Vitamin D and Beta Cells in Type 1 Diabetes: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Multifaceted Roles of Vitamin D for Diabetes: From Immunomodulatory Functions to Metabolic Regulations.Nutrients · 2024Review
- Vitamin D in Autoimmunity: Molecular Mechanisms and Therapeutic Potential.Frontiers in immunology · 2016Review
- The novel role of TRPC6 in vitamin D ameliorating podocyte injury in STZ-induced diabetic rats.Molecular and cellular biochemistry · 2015Article
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Authors and funding
6 authors.
Funding
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Abstract
Type 1 diabetes (T1D) is an autoimmune disease that destroys the insulin-producing beta-islet cells of the pancreas. Currently, there are no treatment modalities for prevention of T1D, and the mechanisms influencing disease inception and early progression are not well understood. We have used the insulin 2(-/-) non-obese diabetic (Ins2(-/-) NOD) model to study stages of T1D and to examine the protective effects of a potent analogue of 1α,25-dihydroxyvitamin D(3), 2α-methyl-19-nor-(20S)-1α,25-dihydroxyvitamin D(3) (2AMD). Pancreatic tissues from control and 2AMD-treated Ins2(-/-) NOD mice were obtained weekly from 5 to 16 weeks of age. Using immunohistochemical (IHC) analysis, samples were analysed for changes in beta cell survival, islet structure and T cell invasion. Weekly intraperitoneal glucose tolerance tests (IPGTT) were performed to assess comparative beta cell function in control and treated animals. IHC demonstrated progressive beta cell destruction in control mice. In contrast, 2AMD treatment preserved islet cell architecture, arrested intra-islet T cell invasion and prevented the transition from insulitis to diabetes. IPGTT results revealed progressive impairment of beta cell function with increasing age in control mice, while 2AMD treatment resulted in normal beta function throughout the study. These results demonstrate that the Ins2(-/-) NOD model provides a rapid and effective method for studying T1D and for assessing efficacy of anti-diabetic agents.
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