The interface between thyroid and diabetes mellitus

Duntas, Leonidas H.; Orgiazzi, Jacques; Brabant, Georg

doi:10.1111/j.1365-2265.2011.04029.x

Cited by 247Thyroid Disorders and TreatmentsDiabetes Management and ResearchDiabetes, Cardiovascular Risks, and Lipoproteins

The interface between thyroid and diabetes mellitus

Duntas, Leonidas H., Orgiazzi, Jacques, Brabant, Georg·2011·Clinical Endocrinology

DOI 10.1111/j.1365-2265.2011.04029.x

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Abstract

Thyroid disease and type 1 but also type 2 diabetes mellitus (DM) are strongly associated, and this has important clinical implications for insulin sensitivity and treatment requirements. The pathophysiological basis of this association has only recently been better elucidated. It rests on a complex interaction of common signalling pathways and, in the case of type 1 diabetes and autoimmune thyroid disease, on a linked genetic susceptibility. The pathophysiological mechanisms underlying this linked regulation are increasingly being unravelled. They are exemplified in the regulation of 5' adenosine monophosphate-activated protein kinase (AMPK), a central target not only for the modulation of insulin sensitivity but also for the feedback of thyroid hormones on appetite and energy expenditure. The present review will discuss these concepts and their consequences for the clinical care of patients with DM and thyroid disorders. Moreover, it makes reference to the added effect of metformin in suppressing TSH.

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Excess thyroid hormones can increase hepatic glucose production through elevated hepatic expression of glucose transporters and enhanced glycogenolysis and gluconeogenesis activities.
“Prior research has shown that excess thyroid hormones can increase hepatic glucose production through the elevated hepatic expression of glucose transporters as well as enhanced glycogenolysis and gluconeogenesis activities (58).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [58]

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Yang, B., Li, J., Haller, M. J., Schatz, D. A., & Rong, L. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1070979 · Cited by 6 · see citing works
“Prior research has shown that excess thyroid hormones can increase hepatic glucose production through the elevated hepatic expression of glucose transporters as well as enhanced glycogenolysis and gluconeogenesis activities (58).”
Background

Authors: Duntas, L. H., Orgiazzi, J., & Brabant, G.
Affiliations: National and Kapodistrian University of Athens (GR)
Hôpital Lyon Sud (FR)
Manchester Academic Health Science Centre (GB)
Corresponding author: Brabant, Georg
ORCID: Duntas, Leonidas H.
Brabant, Georg
Venue: Clinical Endocrinology
Publisher: Wiley
Published: 2011-06-10
Volume: 75
Issue: 1
Pages: 1-9
ISSN: 0300-0664 (ISSN-L)
1365-2265
DOI: 10.1111/j.1365-2265.2011.04029.x
OpenAlex: W2157230369
Cited by: 247
References: 79
Citations by year: 2026: 7 · 2025: 13 · 2024: 15 · 2023: 25 · 2022: 22 · 2021: 18 · 2020: 20 · 2019: 14 · 2018: 19 · 2017: 19 · 2016: 18 · 2015: 19 · 2014: 16 · 2013: 14 · 2012: 6
FWCI: 1.69
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Clinical Endocrinology (publishedVersion)
PubMed (publishedVersion)
Research Explorer (The University of Manchester) (publishedVersion)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords: thyroid dysfunction, type 1 diabetes, type 2 diabetes, autoimmune thyroid disease, insulin sensitivity, AMPK, thyroid hormone feedback, energy expenditure, appetite regulation, genetic susceptibility, metformin, TSH suppression
MeSH terms: Diabetes Mellitus, Humans, Thyroid Diseases

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The interface between thyroid and diabetes mellitus

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