Why Can Insulin Resistance Be a Natural Consequence of Thyroid Dysfunction?

Table 1

Direct effects of T3 on genes that regulate glucose homeostasis at the liver and peripheral tissues (muscle, fat tissue, and fibroblasts).

Gene	Expression	Site	Net effect
glucose-6-phosphatase [5]	Increase	liver	Increase gluconeogenesis and glycogenolysis
protein kinase B (Akt2) [5]	decrease	liver	Decrease glycogen synthesis
β2-adrenergic receptor [5]	Increase	liver	Increase gluconeogenesis and glycogenolysis
inhibitory G protein (Gi) [5]	decrease	liver	Increase gluconeogenesis and glycogenolysis
phosphoenolpyruvate carboxykinase (PEPCK) [6]	Increase	liver	Increase gluconeogenesis
pyruvate carboxylase (PC) [7]	Increase	liver	Increase gluconeogenesis
GLUT2 [8]	Increase	liver	Increase glucose output
malic enzyme [10]	Increase	liver	lipogenesis
Carbohydrate-response element-binding protein (ChREBP) [12]	Increase	liver and fat tissue	lipogenesis
GLUT1 [14]	Increase	peripheral tissues	Increase glucose transport (basal)
GLUT4 [14]	Increase	peripheral tissues	Increase glucose transport (insulin-induced)
β2-adrenergic receptor [20]	Increase	Peripheral tissues	Increase lipolysis
phosphoglycerate kinase (PGK) [15]	Increase	peripheral tissues	Increase glycolysis
Hypoxia-inducible factor 1 (HIF-1α) [15]	Increase	peripheral tissues	Increase glycolysis
PPAR gamma coactivator-1 alpha (PGC-1 alpha) [27]	Increase	peripheral tissues	Increase mitochondrial biogenesis and function
uncoupling protein 3 (UCP3) [17]	Increase	peripheral tissues	Increase mitochondrial energy expenditure