James E. Foley

TL;DR: Obesity, insulin resistance, and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM.

TL;DR: Although enlarged mean subcutaneous abdominal adipocyte size is associated with insulin resistance cross-sectionally, prospectively, both abnormalities are independent and additive predictors of Type II diabetes.

TL;DR: It is demonstrated that both maximal insulin-stimulated glucose transport and utilization, and the sensitivity of the glucose transport system to insulin, was decreased in adipocytes isolated from subjects with NIDDM, consistent with the view that the metabolic alterations observed at the cellular level may contribute to the in vivo insulin resistance of NID DM.

TL;DR: Adipose cellular enlargement is accompanied by the development of a marked "insulin resistance" at the glucose transport level, which may be the consequence of a relative depletion of glucose transport systems in the intracellular pool.

TL;DR: In this article, the authors demonstrate that the improvement in maximal insulin-stimulated glucose transport correlated with the fall in fasting hyperglycemia (r = 0.77, p less than 0.01).