ArticleThe Journal of endocrinology2011
Inositol 1,4,5-trisphosphate receptor 1 mutation perturbs glucose homeostasis and enhances susceptibility to diet-induced diabetes.
Article in The Journal of endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Epigenetic analyses suggest different pathways during pregnancy for development of type 1 diabetes in children with high versus low-neutral human leukocyte antigen-risk.Journal of internal medicine · 2026Article
- Functional genomics reveals mediators of beta cell survival in ER stress and type 2 diabetes risk.bioRxiv : the preprint server for biology · 2026Article
- Integrating genetics with single-cell multiomic measurements across disease states identifies mechanisms of beta cell dysfunction in type 2 diabetes.Nature genetics · 2023Article
- Lack of adipocyte IP3R1 reduces diet-induced obesity and greatly improves whole-body glucose homeostasis.Cell death discovery · 2023Article
- Integration of single-cell multiomic measurements across disease states with genetics identifies mechanisms of beta cell dysfunction in type 2 diabetes.bioRxiv : the preprint server for biology · 2023Article
- MS4A15 drives ferroptosis resistance through calcium-restricted lipid remodeling.Cell death and differentiation · 2022Article
- Cadmium-mediated pancreatic islet transcriptome changes in mice and cultured mouse islets.Toxicology and applied pharmacology · 2021Article
- Cavβ3 Regulates CaDiabetes · 2021Article
- CREB regulates the expression of type 1 inositol 1,4,5-trisphosphate receptors.Journal of cell science · 2021Article
- Review
- The Impact of Sugar-Sweetened Beverage Consumption on the Liver: A Proteomics-based Analysis.Antioxidants (Basel, Switzerland) · 2020Article
- The Endoplasmic Reticulum and Calcium Homeostasis in Pancreatic Beta Cells.Endocrinology · 2020Review
- Metabolic implications of organelle-mitochondria communication.EMBO reports · 2019Review
- Sirolimus induces depletion of intracellular calcium stores and mitochondrial dysfunction in pancreatic beta cells.Scientific reports · 2017Article
- GRP78 haploinsufficiency suppresses acinar-to-ductal metaplasia, signaling, and mutantProceedings of the National Academy of Sciences of the United States of America · 2017Article
- THADA Regulates the Organismal Balance between Energy Storage and Heat Production.Developmental cell · 2017Article
- A Single-Cell Transcriptome Atlas of the Human Pancreas.Cell systems · 2016Article
- Disruption of calcium transfer from ER to mitochondria links alterations of mitochondria-associated ER membrane integrity to hepatic insulin resistance.Diabetologia · 2016Article
- Phosphoinositide signalling in type 2 diabetes: a β-cell perspective.Biochemical Society transactions · 2016Review
- Ankyrin-B metabolic syndrome combines age-dependent adiposity with pancreatic β cell insufficiency.The Journal of clinical investigation · 2015Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The inositol 1,4,5-trisphosphate receptors (IP3Rs) as ligand-gated Ca(2)(+) channels are key modulators of cellular processes. Despite advances in understanding their critical role in regulating neuronal function and cell death, how this family of proteins impact cell metabolism is just emerging. Unexpectedly, a transgenic mouse line (D2D) exhibited progressive glucose intolerance as a result of transgene insertion. Inverse PCR was used to identify the gene disruption in the D2D mice. This led to the discovery that Itpr1 is among the ten loci disrupted in chromosome 6. Itpr1 encodes for IP3R1, the most abundant IP3R isoform in mouse brain and also highly expressed in pancreatic β-cells. To study IP3R1 function in glucose metabolism, we used the Itpr1 heterozygous mutant mice, opt/+. Glucose homeostasis in male mice cohorts was examined by multiple approaches of metabolic phenotyping. Under regular diet, the opt/+ mice developed glucose intolerance but no insulin resistance. Decrease in second-phase glucose-stimulated blood insulin level was observed in opt/+ mice, accompanied by reduced β-cell mass and insulin content. Strikingly, when fed with high-fat diet, the opt/+ mice were more susceptible to the development of hyperglycemia, glucose intolerance, and insulin resistance. Collectively, our studies identify the gene Itpr1 being interrupted in the D2D mice and uncover a novel role of IP3R1 in regulation of in vivo glucose homeostasis and development of diet-induced diabetes.
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Registered trials
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