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Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test
Published on: November 13, 2016
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Radioactive Iodine Therapy and Glucose Tolerance
Roghaieh Samadi1, Babak Shafiei2, Fereidoun Azizi3
1Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Cell Journal
|July 4, 2017
Summary
Radioactive iodine therapy may increase the risk of glucose intolerance. Uptake by the pancreas could damage insulin-producing beta-cells, potentially leading to type 2 diabetes, especially after thyroid cancer treatment.
Area of Science:
- Endocrinology
- Oncology
- Nuclear Medicine
Background:
- Radioactive iodine (RAI) therapy is a standard treatment for thyroid conditions like papillary thyroid carcinoma (PTC) and Graves' disease (GD).
- The sodium-iodide symporter (NIS) facilitates RAI uptake in thyroid cells, but is also expressed in other tissues, including pancreatic islets.
Purpose of the Study:
- To explore the potential link between RAI therapy and the development of glucose intolerance.
- To investigate the implications of RAI uptake in pancreatic beta-cells.
Main Methods:
- Literature review and discussion of existing research on NIS expression and RAI uptake in extrathyroidal tissues.
- Analysis of potential mechanisms by which RAI could affect pancreatic beta-cell function.
Main Results:
- Expression of NIS in pancreatic islets suggests potential for RAI accumulation in beta-cells.
- RAI uptake by beta-cells could lead to cellular damage, impairing insulin production.
Conclusions:
- RAI therapy may pose a risk for glucose intolerance and type 2 diabetes due to potential pancreatic beta-cell damage.
- This risk may be elevated in patients treated with RAI after total thyroidectomy for thyroid cancer.
- Further research is necessary to confirm the association and elucidate the underlying mechanisms.
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