Thyroid hormone excess and glucose intolerance
Abstract
The elevated plasma glucose levels in hyperthyroidism may be explained by increased rates of endogenous glucose production, due mainly to increased gluconeogenesis. The rates of insulin-stimulated glucose disposal in peripheral tissues in hyperthyroidism have been found, in general, either normal or increased. Skeletal muscle is the most important tissue for the disposal of glucose in response to insulin. In this tissue, insulin increases glucose disposal by stimulating glucose transport, glucose phosphorylation/glycolysis, glycogen synthesis and glucose oxidation. Studies examining insulin-stimulated glucose metabolism in skeletal muscle have suggested that, in the hyperthyroid state, it may be of primary importance to increase the rates of glycolysis and lactate formation relative to glucose oxidation in this tissue in order to provide substrate for gluconeogenesis (increase Cori cycle activity). This effect will be achieved primarily by a decrease in glycogen synthesis and an increase in glycogenolysis. When hyperthyroidism becomes more severe, an increased rate of glucose uptake into muscle may then be necessary since the increased conversion of glycogen to lactate could not be sustained for prolonged periods and might lead to a depletion in glycogen stores. This mechanism would ensure that the level of glucose in plasma is kept normal or slightly increased. Thus, an increased Cori cycle activity may be a necessary mechanism to provide optimal conditions in hyperthyroidism for the control of glucose utilization without increasing the risk of hypoglycemia. In addition to lactate, increased rates of gluconeogenesis in hyperthyroidism can also be sustained by increased plasma concentrations of amino acids (mostly glutamine and alanine) and glycerol, as well as by increased plasma concentrations of free fatty acids.
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Increased secretion of insulin is observed in hyperthyroidism.
“Increased secretion of insulin and elevated fasting insulin are observed in hyperthyroidism (60, 61).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [60]
Elevated fasting insulin is observed in hyperthyroidism.
“Increased secretion of insulin and elevated fasting insulin are observed in hyperthyroidism (60, 61).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [60]
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Exogenous Subclinical Hyperthyroidism Impairs Endothelial Function in Nodular Goiter Patients
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“Enhanced gluconeogenesis and glycogenolysis support tissues with sufficient fuel to maintain their energy requirements (Dimitriadis and Raptis, 2001; Klieverik et al., 2008).”
BackgroundSíbio, M. T. D., Luvizotto, R. D. A. M., Olímpio, R. M. C., Corrêa, C. R., Juliana, M., de Oliveira, M., Conde, S. J., Ferreira, A. L. A., Padovani, C. R., & Nogueira, C. R. (2013) · PLoS ONE · doi:10.1371/journal.pone.0056913 · Cited by 25 · see citing works
“It is well established that excess thyroid hormones augment plasma glucose levels [40].”
Dimitriadis, G., Maratou, E., Boutati, E. I., et al. (2008) · European Journal of Endocrinology · doi:10.1530/eje-07-0532 · Cited by 25 · see citing works
“Lactate is of major importance as a substrate in the hyperthyroid state to increase the rate of gluconeogenesis in the liver ( 1 , 31, 32).”
BackgroundInfluentialSelf-citationKarbalaei, N., Noorafshan, A., & Hoshmandi, E. (2016) · Experimental Physiology · doi:10.1113/ep085627 · Cited by 24 · see citing works
“The reason for the impaired glucose tolerance in hyperthyroidism might be because of increased hepatic glucose production, impaired insulin secretion or peripheral insulin insensitivity (Dimitriadis & Raptis, 2001).”
BackgroundTeixeira, S. D. S., Panveloski-Costa, A. C., Carvalho, A., Schiavon, F. P. M., Marques, A. D. C. R., Campello, R. S., Bazotte, R. B., & Nunes, M. T. (2016) · Physiological Reports · doi:10.14814/phy2.12961 · Cited by 23 · see citing works
“It is known that glycogenolysis and gluconeogenesis predominate in hyperthyroid states leading to glucose intolerance (Dimitriadis and Raptis 2001).”
BackgroundMethodInfluentialAl‐Majdoub, M., Lantz, M., & Spégel, P. (2017) · Thyroid · doi:10.1089/thy.2017.0218 · Cited by 23 · see citing works
“Despite the appetite being stimulated, and food intake consequently increased, patients lose weight while also becoming more insulin resistant (1).”
Farasat, T., Cheema, A. M., & Khan, M. N. (2012) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2012.05.017 · Cited by 24 · see citing works
“These observations are in concordance with two previous findings (Dimitriadis & Raptis, 2001; Kim et al., 2002).”
Nutritional and Hormonal Modulation of Adiponectin and its Receptors adipoR1 and adipoR2
de Oliveira, C., de Mattos, A. B. M., Silva, C. B. R., Mota, J. F., & Zemdegs, J. C. S. (2012) · Vitamins and hormones · doi:10.1016/b978-0-12-398313-8.00003-8 · Cited by 23 · see citing works
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Hsieh, Y.-S., Yeh, M.-C., Lin, Y., et al. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1099805 · Cited by 21 · see citing works
“Excess thyroid hormone stimulates lipolysis and the secretion of glucagon, followed by deterioration of glucose metabolism, which can cause glucose intolerance and insulin resistance in T2DM (17).”
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Barmpari, M. E., Kokkorou, M., Micheli, A., et al. (2017) · Journal of Diabetes Research · doi:10.1155/2017/6505814 · Cited by 21 · see citing works
“It is important to diagnose and cure it as soon as possible [51].”
BackgroundDiabetes and thyroid diseases - a review
Sathish, R., & Mohan, V. (2003) · Cited by 20 · see citing works
Thyroid Status in Diabetes Mellitus
Gangte, D. H. D. (2011) · Journal of Glycomics & Lipidomics · doi:10.4172/2153-0637.1000106 · Cited by 19 · see citing works
Hyperthyroidism-Associated Insulin Resistance Is Not Mediated by Adiponectin Levels
Chu, C.-H., Lam, H., Lee, J., et al. (2011) · Journal of Thyroid Research · doi:10.4061/2011/194721 · Cited by 19 · see citing works
“The speed of insulin-stimulated glucose disposal in peripheral tissues is variable in hyperthyroidism and may be normal, increased, or decreased [3].”
Effect of Thyroid Dysfunction on Metabolic Response in Type 2 Diabetic Patients
Mohammad, A. A., Rashidi, M., & Ardakani, A. S. A. (2010) · Iranian journal of diabetes and obesity · Cited by 19 · see citing works
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Santiago, L. A., Santiago, D. A., Faustino, L. C., Cordeiro, A. C. C., Lisboa, P. C., Wondisford, F. E., Pazos-Moura, C. C., & Ortiga-Carvalho, T. M. (2011) · Journal of Endocrinology · doi:10.1530/joe-11-0194 · Cited by 17 · see citing works
“…access TH effects on growth, body composition, and glucose homeostasis have been described and result from the action of TH on different tissues (Dimitriadis & Raptis 2001, Fukuchi et al. 2002, Bassett et al. 2007); however, the molecular mechanisms and the subtype of TR predominantly involved…”
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Endogenous subclinical hyperthyroidism: Metabolic and cardiac parameters
Ψαλτοπούλου, Θ., Ilias, Ι., Toumanidis, S. T., Mantzou, A., Marafelia, P., Gd, P., Koutras, D. A., & Alevizaki, M. K. (2007) · European Journal of Internal Medicine · doi:10.1016/j.ejim.2006.12.010 · Cited by 14 · see citing works
“010 thyroid hormone excess [1–3].”
Venditti, P., Reed, T. T., Víctor, V. M., & Meo, S. D. (2019) · Free Radical Research · doi:10.1080/10715762.2019.1590567 · Cited by 15 · see citing works
“Impaired glucose tolerance in hyperthyroidism has been attributed to several factors, including increased glucose gastrointestinal absorption, post-absorptive hyperglycaemia, high hepatic glucose output, elevated FFA concentrations, impaired insulin secretion, and peripheral insulin insensitivity [98].”
BackgroundLambadiari, V., & Spanoudi, F. (2016) · Journal of Diabetes & Metabolism · doi:10.4172/2155-6156.1000677 · Cited by 12 · see citing works
“There has recently been growing evidence that there might be a range in thyroid hormone values at which insulin sensitivity is optimal, and out of which metabolic disturbances may occur [1,2,5,13].”
BackgroundValidation of Mct8/Oatp1c1 dKO mice as a model organism for the Allan-Herndon-Dudley Syndrome
Maity‐Kumar, G., Ständer, L., Angelis, M. D., Lee, S., Molenaar, A., Becker, L., Garrett, L., Amerie, O. V., Hölter, S. M., Wurst, W., et al. (2022) · Molecular Metabolism · doi:10.1016/j.molmet.2022.101616 · Cited by 12 · see citing works
“In the liver, T3 accelerates de novo glucose production [7 e 9], increases lipolysis [1] and improves cholesterol metabolism by promoting hepatic cholesterol uptake and clearance [1,10].”
- Authors
- Dimitriadis, G., & Raptis, S.
- Affiliations
- National and Kapodistrian University of Athens (GR)
- Venue
- Experimental and Clinical Endocrinology & Diabetes
- Publisher
- Georg Thieme Verlag KG
- Published
- 2001-11-23
- Volume
- 109
- Issue
- Suppl 2
- Pages
- S225-S239
- ISSN
- 0947-7349 (ISSN-L)
- 1439-3646
- OpenAlex
- W2016021698
- Cited by
- 179
- References
- 0
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 3 · 2023: 8 · 2022: 9 · 2021: 8 · 2020: 11 · 2019: 8 · 2018: 11 · 2017: 13 · 2016: 9 · 2015: 7 · 2014: 10 · 2013: 9 · 2012: 6
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental and Clinical Endocrinology & Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- hyperthyroidism, impaired glucose tolerance, hyperglycemia, gluconeogenesis, insulin-stimulated glucose disposal, skeletal muscle glucose metabolism, Cori cycle, glycogenolysis, glycogen synthesis, lactate, hypoglycemia, amino acids, glycerol, free fatty acids
- MeSH terms
- Insulin Secretion, Animals, Gastric Emptying, Glucose, Humans, Insulin, Thyroid Hormones, Glucose Intolerance, Lipid Metabolism
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