Insulin insensitivity of large fat cells.

Large insulin-insensitive adipocytes from adult rats have normal binding capacities and affinities for insulin. Diminished insulin-like responses to spermine and reduced rates of glucose oxidation are also evident in these cells. The results indicate that the defect responsible for this insulin-resistant state exists in a step subsequent to insulin binding, possibly in transmission of the insulin-receptor "signal" since insensitivity occurs under conditions where glucose transport and oxidative processes are not apparently impaired.