Related Experiment Video
Updated: May 13, 2026

Incorporation of a Survivable Liver Biopsy Procedure in Mice to Assess Non-alcoholic Steatohepatitis (NASH) Resolution
Published on: April 16, 2019
Thyroid safety in patients treated with liraglutide
1Oncological Endocrinology, AO Citta' della Salute e della Scienza-Molinette, Via Genova, 3, I-10137 Turin, Italy. mgallo4@cittadellasalute.to.it
New anti-diabetic drugs like liraglutide show no link to thyroid cancer in humans. However, long-term effects of glucagon-like peptide 1 (GLP-1) receptor activation on the human thyroid require further study.
Area of Science:
- Endocrinology
- Pharmacology
- Oncology
Background:
- Novel anti-diabetic drugs, including glucagon-like peptide 1 (GLP-1) analogs, have expanded treatment options for Type 2 diabetes.
- Concerns exist regarding potential cardiovascular and oncological adverse effects of these new therapies.
- Rodent studies with liraglutide suggested a link to medullary thyroid tumors, raising questions about human relevance.
Purpose of the Study:
- To investigate the potential association between liraglutide therapy and thyroid abnormalities in humans.
- To address concerns regarding the oncological safety of GLP-1 receptor agonists.
Main Methods:
- Analysis of sequential changes in plasma calcitonin levels in a large cohort of patients treated with liraglutide.
- Monitoring for the incidence of medullary thyroid cancer in human subjects receiving liraglutide.
Main Results:
- No relationship was identified between liraglutide therapy and plasma calcitonin levels.
- No cases of medullary thyroid cancer were detected in humans treated with liraglutide.
Conclusions:
- Current data suggest liraglutide therapy is not associated with medullary thyroid cancer in humans.
- The long-term impact of sustained GLP-1 receptor activation on the human thyroid remains to be elucidated and warrants further investigation.
Related Concept Videos
Glucagon-like Receptor Agonists
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Graves' Disease I: Introduction
Graves Disease II: Pathophysiology
Hyperthyroidism II: Pathophysiology
Hyperthyroidism I: Introduction
Hypothyroidism II: Pathophysiology

