Journal of Thyroid Research / 2011 / Article / Tab 1

Review Article

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).

GeneExpressionSiteNet effect

glucose-6-phosphatase [5]IncreaseliverIncrease gluconeogenesis and glycogenolysis
protein kinase B (Akt2) [5]decreaseliverDecrease glycogen synthesis
β2-adrenergic receptor [5]IncreaseliverIncrease gluconeogenesis and glycogenolysis
inhibitory G protein (Gi) [5]decreaseliverIncrease gluconeogenesis and glycogenolysis
phosphoenolpyruvate carboxykinase (PEPCK) [6]IncreaseliverIncrease gluconeogenesis
pyruvate carboxylase (PC) [7]IncreaseliverIncrease gluconeogenesis
GLUT2 [8]IncreaseliverIncrease glucose output
malic enzyme [10]Increaseliverlipogenesis
Carbohydrate-response element-binding protein (ChREBP) [12]Increaseliver and fat tissuelipogenesis
GLUT1 [14]Increaseperipheral tissuesIncrease glucose transport (basal)
GLUT4 [14]Increaseperipheral tissuesIncrease glucose transport (insulin-induced)
β2-adrenergic receptor [20]IncreasePeripheral tissuesIncrease lipolysis
phosphoglycerate kinase (PGK) [15]Increaseperipheral tissuesIncrease glycolysis
Hypoxia-inducible factor 1 (HIF-1α) [15]Increaseperipheral tissuesIncrease glycolysis
PPAR gamma coactivator-1 alpha (PGC-1 alpha) [27]Increaseperipheral tissuesIncrease mitochondrial biogenesis and function
uncoupling protein 3 (UCP3) [17]Increaseperipheral tissuesIncrease mitochondrial energy expenditure