What is the Origin of Insulin Resistance Pathophysiology?

The term is a direct combination of the clinical observation (resistance to insulin) and the study of disease process (pathophysiology). Its modern understanding evolved significantly with the elucidation of the insulin signaling cascade, particularly the role of IRS proteins and downstream kinases. It describes a functional decoupling between the hormone signal and the cellular metabolic response.

What is the Mechanism of Insulin Resistance Pathophysiology?

At the cellular level, the mechanism often involves the accumulation of lipid intermediates, such as diacylglycerols, which activate serine kinases. These kinases phosphorylate the insulin receptor substrate (IRS) proteins at inhibitory serine residues rather than the activating tyrosine residues. Consequently, the downstream GLUT4 translocation required for glucose uptake is impaired, leading to intracellular glucose deprivation despite high systemic insulin levels. This molecular interference blocks the normal glucose disposal pathway.

Insulin Resistance Pathophysiology

Meaning

Insulin Resistance Pathophysiology details the molecular and cellular basis by which peripheral tissues, primarily muscle, fat, and liver, exhibit a diminished responsiveness to the actions of circulating insulin. This reduced sensitivity necessitates hyperinsulinemia from the pancreatic beta cells in an attempt to maintain euglycemia, representing a fundamental breakdown in metabolic control. Understanding this pathophysiology is central to managing Type 2 Diabetes and related cardiometabolic syndromes.

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