Cortisol Mediated Insulin Resistance is a pathological state where chronic, excessive levels of the glucocorticoid hormone cortisol interfere with the normal signaling and action of insulin at the cellular level. This interference impairs the peripheral tissues’ ability to efficiently take up glucose, establishing a critical link between chronic stress and metabolic dysfunction. The condition necessitates compensatory hyperinsulinemia from the pancreas to maintain normal blood glucose levels.
Origin
This clinical descriptor combines the stress hormone cortisol with the core metabolic pathology of insulin resistance. It is a well-established concept in endocrinology, underscoring the catabolic and anti-insulin effects of chronically elevated glucocorticoids.
Mechanism
Cortisol promotes insulin resistance primarily by two concurrent actions: it increases hepatic gluconeogenesis, boosting the liver’s glucose output, and it impairs the proper function and translocation of GLUT4 glucose transporters in muscle and fat cells. This sustained hormonal antagonism disrupts the normal cellular response to insulin, contributing to persistent hyperglycemia and the eventual failure of pancreatic beta cells.
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