Ectopic fat in insulin resistance, dyslipidemia, and cardiometabolic disease: Reply

摘要

Shin and Lee discuss the potential role of increased levels of glucose and advanced glycation end products on the insulin receptor and the development of insulin resistance. Although there are many hypotheses for the pathogenesis of insulin resistance in the liver and in skeletal muscle, increased levels of advanced glycation end products, unlike increased levels of ectopic lipid, would not explain the occurrence of insulin resistance in normoglycemic persons who are at increased risk for the development of type 2 diabetes.