Insulin resistance is thought to involve a defect in insulin signalling at the level of IRS or Akt signalling. Since this pathway controls numerous actions of insulin including  glucose disposal, protein synthesis and lypolysis it is logical then that all such pathways should be disrupted in the insulin resistant state. However we have recently shown that changes in Akt signalling do not necessarily translate into defective insulin action and so we wanted to examine how broad insulin resistance is in regard to the many metabolic effects of this hormone.  Therefore we have undertaken a systematic approach to examine insulin signalling in combination with insulin regulated glucose transport, anti-lipolysis and protein synthesis in a range of models of insulin resistance in 3T3-L1 adipose and in adipose tissue from animals subjected to diet induced obesity.  Insulin regulated glucose transport was impaired in all models of insulin resistance. Intriguingly, while insulin regulated Akt phosphorylation was defective in all insulin resistance models, decreased insulin-stimulated glucose transport was the only consistent defect observed from various parameters measured. These data indicate that insulin resistance in adipose tissue is highly selective for glucose transport and likely involves a defect in a component that is highly specific to this pathway. One of the important implications of this work is that those pathways not defective in the insulin resistant state may undergo hyper activation under the influence of the compensatory hyperinsulinemic often observed under these conditions.