Research
Hormonal
Type 3 Deiodinase (D3) inactivation of thyroid hormone is essential for pancreatic beta-cell maturation and insulin secretion; D3 deficiency leads to glucose intolerance and impaired insulin secretion.
Proper regulation of thyroid hormone inactivation (by D3) in the pancreas is crucial for normal insulin secretion. Disruption of this local balance can impair beta-cell function and contribute to glucose intolerance, independent of systemic thyroid status.
GoodSupportsHIGH confidence
D3KO mice exhibited a glucose intolerant phenotype due to impaired glucose-stimulated insulin secretion, reduced size, and absolute mass of pancreatic islet and beta-cells, decreased insulin content, and reduced expression of key genes involved in glucose sensing, insulin synthesis, and exocytosis.
Why this rating
Based on D3KO mouse models showing clear glucose intolerance.
Source
Metabolic Effects of the Intracellular Regulation of Thyroid Hormone: Old Players, New Concepts
Annunziata Gaetana Cicatiello et al. · Frontiers in Endocrinology · 2018
DOI 10.3389/fendo.2018.00474
narrative_reviewCited 177×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Intracellular regulation of thyroid hormone by deiodinases (D1, D2, D3) dictates tissue-specific metabolic outcomes, where local T3 activation promotes energy expenditure and lipid mobilization, while inactivation preserves energy stores.Good
- Brown Adipose Tissue (BAT) activity and adaptive thermogenesis are critically dependent on local Type 2 Deiodinase (D2) activity converting T4 to T3, particularly in response to cold exposure.Good
- Local thyroid hormone activation in skeletal muscle via D2 drives a shift from slow-twitch (Type I) to fast-twitch (Type II) fibers, increasing energy expenditure and influencing insulin sensitivity.Good
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