Key result
Thyroid dysfunction and type 2 diabetes share bidirectional links driven primarily by insulin resistance.
Answers are grounded in this paper and cite their sources.
There is an overwhelming evidence of the relationship between type 2 diabetes mellitus (T2DM) and thyroid dysfunction. The literature is robustly littered with data demonstrating the intersection of these two most common endocrine conditions. However, the extent of these intersections still remains complex, conflicting, and unclear. Therefore, we aimed to review the current literature on these intersections with an emphasis on interrelationship between thyroid dysfunction and T2DM. Several mechanisms have been postulated; some of which include but are not limited to blunting of the nocturnal thyroid-stimulating hormone (TSH) peak impairment of the TSH response to TRH from the hypothalamus, impairment of peripheral conversion from T4 to T3, increased hepatocyte plasma membrane concentrations of glucose transporter in the liver, which leads to an increased hepatic glucose output and abnormal glucose metabolism, to the perturbed genetic expression of a group of genes along with physiological abnormality. Insulin resistance has been shown to be associated with thyroid dysfunction (hyperthyroidism) in patients with T2DM. In other words, insulin resistance links both conditions. Several studies have evidenced an incontrovertible role of thyroid dysfunction as an intertwined cohort of T2DM. A plethora of guidelines have been exhaustively evaluated highlighting their key messages while synthesizing the relationship existing between them. The different treatment options available inexorably validate the importance of the intersection between these two endocrine conditions.
No takes yet. Share an insight, caveat, or question.
Ezeani et al. (2022) conducted a review in Type 2 diabetes mellitus and thyroid dysfunction. Thyroid dysfunction was evaluated. Thyroid dysfunction and type 2 diabetes mellitus share a complex interrelationship linked by insulin resistance, altered TSH regulation, impaired T4-to-T3 conversion, and hepatic glucose output.
Synapse has enriched 10 related papers. Consider them for comparative context: