Insulin resistance and diabetes in hyperthyroidism: a possible role for oxygen and nitrogen reactive species

Abstract

In addition to insulin, glycemic control involves thyroid hormones. However, an excess of thyroid hormone can disturb the blood glucose equilibrium, leading to alterations of carbohydrate metabolism and, eventually, diabetes. Indeed, experimental and clinical hyperthyroidism is often accompanied by abnormal glucose tolerance. A common characteristic of hyperthyroidism and type 2 diabetes is the altered mitochondrial efficiency caused by the enhanced production of reactive oxygen and nitrogen species. It is known that an excess of thyroid hormone leads to increased oxidant production and mitochondrial oxidative damage. It can be hypothesised that these species represent the link between hyperthyroidism and development of insulin resistance and diabetes, even though direct evidence of this relationship is lacking. In this review, we examine the literature concerning the effects of insulin and thyroid hormones on glucose metabolism and discuss alterations of glucose metabolism in hyperthyroid conditions and the cellular and molecular mechanisms that may underline them.

Keywords:

• Diabetes
• hyperthyroidism
• insulin resistance
• insulin secretion
• reactive nitrogen species (RNS)
• reactive oxygen species (ROS)

Acknowledgements

The authors thank Brian Normanly (University of Valencia-CIBERehd) for his editorial assistance.

Disclosure statement

No potential conflict of interest was reported by the authors that could be perceived as prejudicing the impartiality of this review.

Additional information

Funding

This work was supported by grants from Italian Ministry of University and Scientific and Technological Research and grants PI16/1083 from Carlos III Health Institute and from the European Regional Development Fund (ERDF “A way to build Europe”).