L. Rossetti

TL;DR: The data demonstrate that a reduction of beta-cell mass leads to the development of insulin resistance, and correction of hyperglycemia with phlorizin, without change in insulin levels, normalizes insulin sensitivity.

TL;DR: Chronic hyperglycemia can lead to a defect in in vivo insulin secretion which is reversible when normoglycemia is restored, and normalization of the plasma glucose profile by phlorizin treatment in diabetic rats completely corrected all three beta cell abnormalities.

TL;DR: Data suggest that glucose transport is the major determinant of glucose disposal at low insulin concentration, while the rate-limiting step shifts to an intracellular site at high physiological insulin concentration; and prolonged moderate hyperglycemia and hypoinsulinemia determine two distinct cellular defects in skeletal muscle at the levels of glucose transport/phosphorylation and glycogen synthesis.

TL;DR: Investigating how normalization of glycemia without insulin therapy in diabetic rats influences 3-O-methylglucose transport and the expression and translocation of two genetically distinct species of glucose transporters (GTs) in adipose cells results in changes in GT functional activity.

TL;DR: Findings suggest a defect early in the pathway of glucose utilization, probably at the step of glucose transport, reflects impaired glucose transporter translocation or intrinsic activity in response to diabetes.