Trial reportThe Journal of clinical endocrinology and metabolism2020
Thyroid Hormone Effects on Glucose Disposal in Patients With Insulin Receptor Mutations.
Trial report in The Journal of clinical endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02457897 (Thyroid Hormone to Induce Non-Insulin Mediated Glucose Disposal in Patients With Insulin Receptor Mutations), which is not on this map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Thyroid Hormone to Induce Non-Insulin Mediated Glucose Disposal in Patients With Insulin Receptor Mutations
Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Free fatty acid processing diverges in human pathologic insulin resistance conditions.The Journal of clinical investigation · 2020Trial
- Inverse Association Between the Dawn Phenomenon and Thyroid Feedback Quantile-Based Index in Type 2 Diabetes Using Continuous Glucose Monitoring: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Elucidating the effect of levothyroxine and triiodothyronine on methylglyoxal derived stress.Endocrine · 2025Article
- Thermogenic adipose tissue in energy regulation and metabolic health.Frontiers in endocrinology · 2023Review
- Advance in the Correlation between Diabetic Nephropathy and Abnormal Serum Thyroid Hormone Levels in Patients.Emergency medicine international · 2023Article
- Activating Human Adipose Tissue with the β3-Adrenergic Agonist Mirabegron.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Energy expenditure due to gluconeogenesis in pathological conditions of insulin resistance.American journal of physiology. Endocrinology and metabolism · 2021Article
- Therapeutic Perspectives of Thermogenic Adipocytes in Obesity and Related Complications.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
contextPatients with mutations of the insulin receptor gene (INSR) have extreme insulin resistance and are at risk for early morbidity and mortality from diabetes complications. A case report suggested that thyroid hormone could improve glycemia in INSR mutation in part by increasing brown adipose tissue (BAT) activity and volume.
objectiveTo determine if thyroid hormone increases tissue glucose uptake and improves hyperglycemia in INSR mutation.
designSingle-arm, open-label study of liothyronine.
settingNational Institutes of Health.
participantsPatients with homozygous (n = 5) or heterozygous (n = 2) INSR mutation.
interventionLiothyronine every 8 hours for 2 weeks (n = 7); additional 6 months' treatment in those with hemoglobin A1c (HbA1c) > 7% (n = 4). OUTCOMES: Whole-body glucose uptake by isotopic tracers; tissue glucose uptake in muscle, white adipose tissue (WAT) and BAT by dynamic [18F] fluorodeoxyglucose positron emission tomography/computed tomography; HbA1c.
resultsThere was no change in whole-body, muscle, or WAT glucose uptake from baseline to 2 weeks of liothyronine. After 6 months, there was no change in HbA1c (8.3 ± 1.2 vs 9.1 ± 3.0%, P = 0.27), but there was increased whole-body glucose disposal (22.8 ± 4.9 vs 30.1 ± 10.0 µmol/kg lean body mass/min, P = 0.02), and muscle (0.7 ± 0.1 vs 2.0 ± 0.2 µmol/min/100 mL, P < 0.0001) and WAT glucose uptake (1.2 ± 0.2 vs 2.2 ± 0.3 µmol/min/100 mL, P < 0.0001). BAT glucose uptake could not be quantified because of small volume. There were no signs or symptoms of hyperthyroidism.
conclusionLiothyronine administered at well-tolerated doses did not improve HbA1c. However, the observed increases in muscle and WAT glucose uptake support the proposed mechanism that liothyronine increases tissue glucose uptake. More selective agents may be effective at increasing tissue glucose uptake without thyroid hormone-related systemic toxicity.Clinical Trial Registration Number: NCT02457897; https://clinicaltrials.gov/ct2/show/NCT02457897.
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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.