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Free Radic Res. 2019 Mar;53(3):248-268. doi: 10.1080/10715762.2019.1590567. Epub 2019 Mar 25.

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

Author information

1
a Dipartimento di Biologia , Università di Napoli Federico II , Napoli , Italy.
2
b Department of Chemistry , Eastern Kentucky University , Richmond , KY , USA.
3
c Service of Endocrinology, Dr. Peset University Hospital, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO) , Valencia , Spain.
4
d Department of Physiology , University of Valencia , Valencia , Spain.

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)

PMID:
30843740
DOI:
10.1080/10715762.2019.1590567
[Indexed for MEDLINE]

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