Androgen receptor mutations in familial androgen insensitivity syndrome: A metabolic reprogramming pathway to type 2 diabetes susceptibility

Table 2 Organ-specific differences in androgen - receptor signaling

Organ/tissue	Principal action of AR	Metabolic consequences when AR signaling is impaired
Skeletal muscle	Drives glucose utilization and myofiber growth	AR loss impairs glycolysis and diminishes insulin sensitivity
Liver	Promotes fattyacid oxidation and enhances insulin responsiveness	AR deficiency predisposes to hepatic steatosis and insulin resistance
Adipose tissue	Restrains visceralfat accumulation and regulates lipid turnover	Lack of adipocyte AR increases visceral obesity and insulin resistance
Pancreatic βcells	Potentiates glucosestimulated insulin secretion	AR activation boosts insulin release, whereas AR knockout blunts excessive secretion
Hypothalamic neurons	Preserves wholebody insulin sensitivity	Neuronal AR deletion elicits hypothalamusdriven insulin resistance

AR: Androgen receptor; β cells: Beta cells (insulin-producing cells in the pancreas).