Prediabetes represents an intermediate state of hyperglycemia reflecting progressive insulin resistance and beta-cell dysfunction that has not yet reached the diagnostic threshold for type 2 diabetes. The pathophysiology involves two concurrent defects. First, insulin resistance develops primarily in skeletal muscle, liver, and adipose tissue: excess visceral adiposity promotes chronic low-grade inflammation through adipokine dysregulation (increased TNF-alpha, IL-6, resistin; decreased adiponectin), which impairs insulin receptor substrate (IRS) phosphorylation and downstream PI3K/Akt signaling, reducing glucose transporter type 4 (GLUT4) translocation to cell membranes. In the liver, insulin resistance disinhibits hepatic gluconeogenesis, producing excessive glucose output even in the fasting state — this is the mechanism underlying impaired fasting glucose (IFG, fasting glucose 5.5–6.9 mmol/L). Second, pancreatic beta-cell compensation gradually fails: initially, beta cells compensate for peripheral insulin resistance by increasing insulin secretion (hyperinsulinemia), maintaining near-normal glucose levels for years. Over time, beta-cell mass declines through glucotoxicity, lipotoxicity, and amyloid deposition (islet amyloid polypeptide, or amylin, co-secreted with insulin forms toxic oligomers that induce beta-cell apoptosis). By the time of prediabetes diagnosis, approximately 50-80% of beta-cell function has already been lost. Impaired glucose...