Insulin Resistance
Diminished biological response of target tissues (liver, muscle, adipose) to insulin, requiring higher insulin concentrations to maintain euglycemia and underlying type 2 diabetes, metabolic syndrome, and NAFLD.
Insulin resistance is driven by adipose tissue dysfunction, ectopic lipid deposition (intramyocellular and hepatic lipids), low-grade inflammation, and altered gut microbiota. Quantification: HOMA-IR ≥ 2.5 suggests resistance; gold-standard is hyperinsulinemic-euglycemic clamp. MNHD repeatedly frames many chronic disease chapters (NAFLD, PCOS, T2D, cardiovascular disease, certain cancers) on a shared insulin-resistance axis.
How each textbook covers it
Krause and Mahan's Food and the Nutrition Care Process, 16th ed. — Chapter 30
A central feature of T2DM, NAFLD, PCOS, and metabolic syndrome. Driven by visceral adiposity, chronic low-grade inflammation, ectopic lipid deposition, and lifestyle factors. Surrogate measures include HOMA-IR and fasting insulin. Improves with weight loss, physical activity, Mediterranean diet, and certain medications (metformin, GLP-1 agonists, SGLT2 inhibitors).
Modern Nutrition in Health and Disease, 12th ed. — Ch 63: Nutrition Management of Diabetes
Insulin resistance is driven by adipose tissue dysfunction, ectopic lipid deposition (intramyocellular and hepatic lipids), low-grade inflammation, and altered gut microbiota. Quantification: HOMA-IR ≥ 2.5 suggests resistance; gold-standard is hyperinsulinemic-euglycemic clamp. MNHD repeatedly frames many chronic disease chapters (NAFLD, PCOS, T2D, cardiovascular disease, certain cancers) on a shared insulin-resistance axis.
Related terms
Metabolic Syndrome, Metabolic syndrome, NAFLD, Type 2 Diabetes Mellitus, Type 2 diabetes, mTORC1