Precision Insights into Insulin Resistance: From Mechanisms and Symptoms to Quantitative Detection

Precision Insights into Insulin Resistance: From Mechanisms and Symptoms to Quantitative Detection

What Is Insulin Resistance?

Insulin resistance refers to a state of reduced tissue sensitivity to insulin, such that the insulin secreted by the pancreas fails to effectively promote glucose uptake and utilization in peripheral tissues—including muscle, adipose tissue, and the liver. To maintain blood glucose homeostasis, pancreatic β-cells compensatorily secrete larger amounts of insulin, leading to hyperinsulinemia. Over time, this chronic state progressively exhausts the pancreatic reserve capacity, eventually advancing to impaired glucose tolerance and ultimately type 2 diabetes mellitus. At the molecular level, core defects in insulin resistance typically involve aberrant phosphorylation of insulin receptor substrates, impaired activation of the PI3K/Akt signaling cascade, and interference from pro-inflammatory cytokines such as TNF-α and IL-6—all of which collectively constitute the pathophysiological foundation of metabolic dysregulation.