Jerrold M. Olefsky

TL;DR: During each insulin infusion, hepatic glucose output was virtually 100% suppressed in all 3 groups, and the dose-response curve for insulin stimulation of glucose disposal in well controlled and poorly controlled diabetic subjects was significantly right-shifted.

TL;DR: It is found that disruption of the IR/IRS-1 interaction has no effect upon translocation of the insulin-responsive glucose transporter (GLUT4) and this suggests that phosphorylated IRS-1 is not an essential component of the metabolic insulin signaling pathway that leads to GLUT4 translocation.

TL;DR: A time-dependent slowing of the overall insulin dissociation rate was observed as the length of the association phase increased, and this phenomenon is independent of a number of intracellular processes studied and is inherent in the plasma membrane.

TL;DR: Evidence is found that adipocyte insulin receptors exhibit similar properties to those originally described by De Meyts et al. for other insulin receptor systems, and under conditions where the accelerating effect of native insulin is either not appreciable or is maximal, 125I-insulin does not dissociate from its receptors as a first order process, suggesting that, even in the absence of negatively cooperative effects, adipocytes do not behave as a kinetically homogeneous population.

TL;DR: ABSTRACT β-arrestin-1 is an adaptor protein that mediates agonist-dependent internalization and desensitization of G-protein-coupled receptors (GPCRs) and also participates in the process of heterologous desensITization between receptor tyrosine kinases and GPCR signaling.