P-83: Alternative pathways of manifesting the rapidmetabolic effects of insulin

Summary

Our long term studies on the insulin-like effects of vanadium salts [ref. 1 - 6] have taught us that the rapid metabolic effects of insulin can be fully manifested through mechanisms not involving insulin-receptor activation, nor tyrosyl phosphorylation of insulin-receptor substrate 1 (IRS-1). This is valid for a variety of metabolic effects that do not share a common mechanistic pathway, such as activation of hexose uptake, enhancing glucose metabolism, and inhibiting lipolysis. The key players of this alternative back-up system are specific protein-phosphotyrosine phosphatases (PTPases) and non-receptor protein-tyrosine kinases of cytosolic and of plasma-membrane origin [7-9], and manuscripts in preparation). The establishment of a cell-free experimental system [i.e. ref. 10] now assists the elucidation of “cross-talk” relationships between the key components of this alternative backup system.