ArticleEndocrinology2011
The thyroid hormone-inactivating type III deiodinase is expressed in mouse and human beta-cells and its targeted inactivation impairs insulin secretion.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.Thyroid : official journal of the American Thyroid Association · 2014Guideline
- Peripheral manifestations of monocarboxylate transporter 8 deficiency: hepatic and skeletal muscle involvement.Frontiers in pediatrics · 2026Review
- Gene polymorphisms and thyroid hormone signaling: implication for the treatment of hypothyroidism.Endocrine · 2024Review
- Sustained Pituitary T3 Production Explains the T4-mediated TSH Feedback Mechanism.Endocrinology · 2023Article
- Preventive Effect of Molecular Iodine in Pancreatic Disorders from Hypothyroid Rabbits.International journal of molecular sciences · 2023Article
- Developmental thyroid hormone action on pro-opiomelanocortin-expressing cells programs hypothalamic BMPR1A depletion and brown fat activation.Journal of molecular cell biology · 2023Article
- Selenium status and type 2 diabetes risk.Archives of biochemistry and biophysics · 2022Review
- DIO3 protects against thyrotoxicosis-derived cranio-encephalic and cardiac congenital abnormalities.JCI insight · 2022Article
- Thyroid Hormone Deiodinases: Dynamic Switches in Developmental Transitions.Endocrinology · 2021Review
- Deiodinases and the Metabolic Code for Thyroid Hormone Action.Endocrinology · 2021Review
- Genetically Determined Higher TSH Is Associated With a Lower Risk of Diabetes Mellitus in Individuals With Low BMI.The Journal of clinical endocrinology and metabolism · 2021Article
- Selenocysteine insertion sequence binding protein 2 (Sbp2) in the sex-specific regulation of selenoprotein gene expression in mouse pancreatic islets.Scientific reports · 2020Article
- Selenoprotein F knockout leads to glucose and lipid metabolism disorders in mice.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020Article
- Relationship between Free Thyroxine and Islet Beta-cell Function in Euthyroid Subjects.Current medical science · 2020Article
- Genomic imprinting and its effects on postnatal growth and adult metabolism.Cellular and molecular life sciences : CMLS · 2019Review
- Paradigms of Dynamic Control of Thyroid Hormone Signaling.Endocrine reviews · 2019Review
- The Deiodinase Trio and Thyroid Hormone Signaling.Methods in molecular biology (Clifton, N.J.) · 2018Review
- The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology.International journal of endocrinology · 2018Review
- Metabolic Effects of the Intracellular Regulation of Thyroid Hormone: Old Players, New Concepts.Frontiers in endocrinology · 2018Review
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Deiodinases are selenoproteins that activate or inactivate thyroid hormone. During vertebrate development, these pathways control thyroid hormone action in a cell-specific fashion explaining how systemic thyroid hormone can affect local control of tissue embryogenesis. Here we investigated the role of the thyroid hormone-inactivating deiodinase (D3) in pancreatic islet function and glucose homeostasis. D3 expression was determined by real-time PCR, immunofluorescence, and enzyme activity. Embryonic and adult wild-type mice and Mice with targeted disruption of Dio3 gene (D3KO) as well as human fetal pancreas and adult islets were studied. Insulin secretion was evaluated in adult mouse isolated islets. We found Dio3 gene expression and protein highly expressed in embryonic and adult pancreatic islets, predominantly in β-cells in both humans and mice. However, mRNA levels were barely detectable for both the thyroid hormone-activating deiodinases types 1 and 2. D3KO animals were found to be glucose intolerant due to in vitro and in vivo impaired glucose-stimulated insulin secretion, without changes in peripheral sensitivity to insulin. D3KO neonatal (postnatal day 0) and adult pancreas exhibited reduced total islet area due to reduced β-cell mass, insulin content, and impaired expression of key β-cells genes. D3 expression in perinatal pancreatic β-cells prevents untimely exposure to thyroid hormone, the absence of which leads to impaired β-cell function and subsequently insulin secretion and glucose homeostasis. An analogous role is likely in humans, given the similar D3 expression pattern.
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Registered trials
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.