Figure 1. Schematic representation of selective postreceptor (partial) hepatic insulin resistance.

In insulin-resistant states in mice, the ability of insulin to suppress hepatic gluconeogenesis is impaired (dashed red arrows), whereas insulin-stimulated de novo lipogenesis is increased (solid green arrows) (5). Only selected signaling intermediaries are shown. INSR, insulin receptor. Asterisks indicate signaling components in which human genetic defects have been reported to date.