A Vanadyl Sulfate-Bovine Serum Albumin Complex Stimulates the Release of Lipoprotein Lipase Activity from Isolated Rat Fat Pads through an Increase in the Cellular Content of cAMP and myo-Inositol 1, 4, 5-Trisphosphate

Abstract

A vanadyl sulfate-bovine serum albumin complex (vanadyl-BSA) prolonged the stability of the V⁴⁺ oxidation state, although vanadyl alone can readily change the oxidation state from V⁴⁺ to V⁵⁺ under physiological conditions. Vanadyl-BSA stimulated the release of lipoprotein lipase (LPL) acitivty from isolated rat fat pads and increased the cellular LPL activity in a time-dependent manner. These effects were independent of protein synthesis. Propranolol, quin 2-AM, ruthenium red, and neomycin all inhibited LPL release more potently than the increase in activity. In contrast, potent inhibition of the increase effect was observed with genistein and wortmannin. Short-term incubation of the fat pads with vanadyl-BSA showed a transient increase in the cellular content of cAMP and myo-inositol 1, 4, 5-triphosphate (IP₃), which was inhibited by propranolol and neomycin, respectively. These results suggest that vanadyl-BSA stimulates the release of LPL activity through an increase in the cellular content of cAMP and IP₃, leading to an increased intracellular Ca²⁺ concentration, and tat it also increases cellular LPL activity via process(es) sensitive to genistein and wortmanni.