Glucose metabolism in anterior pituitary adenomas

Abstract

Glucose metabolism alterations are frequently observed in patients with secretory pituitary adenomas. The most commonly secreted hormones in these tumors include prolactin, growth hormone (GH), adrenocorticotropic hormone (ACTH), and thyroid-stimulating hormone (TSH), all of which can disrupt glucose homeostasis through distinct pathophysiological mechanisms. Prolactin stimulates pancreatic β-cell proliferation, enhances insulin gene transcription, increases intracellular insulin content, and augments glucose-induced insulin secretion. GH promotes lipolysis and hepatic glucose production while impairing peripheral glucose uptake, contributing to insulin resistance. ACTH, via excess glucocorticoids, reduces GLUT-4 translocation, enhances gluconeogenesis and proteolysis, and inhibits glycogen synthesis. Excessive TSH leads to increased T3 and T4 production, which in turn stimulate glucose uptake in muscle and enhance both glycolysis and gluconeogenesis. This review summarizes the current understanding of how hormone hypersecretion in pituitary adenomas contributes to glucose metabolism dysregulation.