ArticleThe Journal of biological chemistry2011
Aryl hydrocarbon receptor nuclear translocator/hypoxia-inducible factor-1{beta} plays a critical role in maintaining glucose-stimulated anaplerosis and insulin release from pancreatic {beta}-cells.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- Aryl hydrocarbon receptor nuclear translocator limits the recruitment and function of regulatory neutrophils against colorectal cancer by regulating the gut microbiota.Journal of experimental & clinical cancer research : CR · 2023Article
- Insight into the physiological and pathological roles of the aryl hydrocarbon receptor pathway in glucose homeostasis, insulin resistance, and diabetes development.Cellular & molecular biology letters · 2022Review
- LncRNA MALAT1 Promotes PPARα/CD36-Mediated Hepatic Lipogenesis in Nonalcoholic Fatty Liver Disease by Modulating miR-206/ARNT Axis.Frontiers in bioengineering and biotechnology · 2022Article
- Isoform-specific Roles of Prolyl Hydroxylases in the Regulation of Pancreatic β-Cell Function.Endocrinology · 2022Article
- INFIMA leverages multi-omics model organism data to identify effector genes of human GWAS variants.Genome biology · 2021Article
- Endothelial Aryl Hydrocarbon Receptor Nuclear Translocator Mediates the Angiogenic Response to Peripheral Ischemia in Mice With Type 2 Diabetes Mellitus.Frontiers in cell and developmental biology · 2021Article
- Diabetic atherosclerosis: is there a role for the hypoxia-inducible factors?Bioscience reports · 2020Review
- The Loss of ARNT/HIF1β in Male Pancreatic β-Cells Is Protective Against High-Fat Diet-Induced Diabetes.Endocrinology · 2019Article
- A HIF-LIMD1 negative feedback mechanism mitigates the pro-tumorigenic effects of hypoxia.EMBO molecular medicine · 2018Article
- Role of prolyl hydroxylase domain proteins in the regulation of insulin secretion.Physiological reports · 2016Article
- Metabolomics applied to the pancreatic islet.Archives of biochemistry and biophysics · 2016Review
- Deletion of ARNT/HIF1β in pancreatic beta cells does not impair glucose homeostasis in mice, but is associated with defective glucose sensing ex vivo.Diabetologia · 2015Article
- The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling.Carcinogenesis · 2015Review
- Molecular network-based analysis of guizhi-shaoyao-zhimu decoction, a TCM herbal formula, for treatment of diabetic peripheral neuropathy.Acta pharmacologica Sinica · 2015Article
- Article
- Mitochondrial metabolism of pyruvate is essential for regulating glucose-stimulated insulin secretion.The Journal of biological chemistry · 2014Article
- Silencing of hypoxia-inducible factor-1β induces anti-tumor effects in hepatoma cell lines under tumor hypoxia.PloS one · 2014Article
- Toxicological function of adipose tissue: focus on persistent organic pollutants.Environmental health perspectives · 2013Review
- Decreased serum glucose and glycosylated hemoglobin levels in patients with Chuvash polycythemia: a role for HIF in glucose metabolism.Journal of molecular medicine (Berlin, Germany) · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The metabolic pathways that are involved in regulating insulin secretion from pancreatic β-cells are still incompletely understood. One potential regulator of the metabolic phenotype of β-cells is the transcription factor aryl hydrocarbon receptor nuclear translocator (ARNT)/hypoxia-inducible factor (HIF)-1β. ARNT/HIF-1β levels are profoundly reduced in islets obtained from type 2 diabetic patients. However, no study to date has investigated key pathways involved in regulating insulin release in β-cells that lack ARNT/HIF-1β. In this study, we confirm that siRNA-mediated knockdown of ARNT/HIF-1β inhibits glucose-stimulated insulin secretion. We next investigated the metabolic consequence of the loss of ARNT/HIF-1β knockdown. We demonstrate that β-cells with reduced ARNT/HIF-1β expression levels exhibit a 31% reduction in glycolytic flux without significant changes in glucose oxidation or the ATP:ADP ratio. Metabolic profiling of β-cells treated with siRNAs against the ARNT/HIF-1β gene revealed that glycolysis, anaplerosis, and glucose-induced fatty acid production were down-regulated, and all are key events involved in glucose-stimulated insulin secretion. In addition, both first and second phase insulin secretion in islets were significantly reduced after ARNT/HIF-1β knockdown. Together, our data suggest an important role for ARNT/HIF-1β in anaplerosis, and it may play a critical role in maintaining normal secretion competence of β-cells.
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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.