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RESEARCH PRODUCT

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

Victor M. VictorPaola VendittiTanea T. ReedSergio Di Meo

subject

0301 basic medicinemedicine.medical_specialtyendocrine systemendocrine system diseasesmedicine.medical_treatmentDiabetes hyperthyroidism insulin resistance insulin secretion reactive nitrogen species (RNS) reactive oxygen species (ROS)Type 2 diabetesCarbohydrate metabolismBiochemistryHyperthyroidism03 medical and health sciencesInsulin resistanceDiabetes mellitusInternal medicinemedicineHumansGlycemic030102 biochemistry & molecular biologyChemistryInsulinThyroidGeneral Medicinemedicine.diseaseReactive Nitrogen SpeciesOxygen030104 developmental biologymedicine.anatomical_structureEndocrinologyDiabetes Mellitus Type 2Insulin ResistanceReactive Oxygen SpeciesHormone

description

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.

10.1080/10715762.2019.1590567https://pubmed.ncbi.nlm.nih.gov/30843740