Metabolic changes in type 2
diabetes The metabolic abnormalities of type 2 diabetes q mellitus are the result of
insulin resistance expressed primarily in liver, muscle, and adipose tissue :
1)
Hyperglycemia: Hyperglycemia is caused by
increased hepatic production of glucose, combined with diminished peripheral
use. Ketosis is usually minimal or absent in type 2 patients because the
presence of insulin—even in the presence of insulin resistance—diminishes
hepatic ketogenesis. [Note: Metformin, an oral agent for the treatment of type
2 diabetes, inhibits hepatic gluconeogenesis1.] 2) Dyslipidemia: In the liver, fatty acids are converted to triacylglycerols, which are packaged and secreted in VLDL. Chylo microns are synthesized from dietary lipids by the intestinal mucosal cells following a meal (see p. 177). Because lipoprotein degradation catalyzed by lipoprotein lipase in adipose tissue (and muscle, see p. 228) is low in diabetics, the plasma chylomicron and VLDL levels are elevated, resulting in hypertriacylglycerolemia. Low HDL levels are also associated with type 2 diabetes.
