• Shamoon, Harry (PI)
  • Rossetti, Luciano (PI)

Project: Research project

Project Details


Insulin resistance is a common characteristic of the diabetic state and of
several other pathological conditions, such as hypertension and obesity.
Over the last several years, numerous reports have demonstrated the in
vitro and in vivo insulin-like activity of vanadate salts. Particularly,
vanadate has been shown to stimulate glucose uptake and glycogen synthase
activity in hepatocytes, adipocytes, diaphragm and skeletal muscle.
Recently, we have demonstrated that the oral administration of vanadate
salts improves glucose tolerance and completely normalizes insulin-
mediated glucose uptake in diabetic animals, primarily through the
stimulation of skeletal muscle glycogen synthesis. These and other
previous observations support the hypothesis that this trace element can
potentiate insulin action at the cellular level and that trace element
therapy, either alone or in combination, may prove effective in the
treatment of human diabetes mellitus. Insulin maintains glucose
homeostasis by two major mechanisms: a) suppression of hepatic glucose
production; b) stimulation of peripheral (muscle) glucose uptake. Once
glucose is transported into the cell, it is phosphorylated to glucose 6-
phosphate (G-6-P) and enters one of two major pathways, glycogen synthesis
and glycolysis. In turn, glycolysis leads either to lactate formation or
pyruvate oxidation in the Krebs cycle Recently, techniques have been
developed to measure in vivo the rates of insulin-mediated glucose
metabolism in humans. Thus, in the present study, we propose to examine
the effect of the oral administration of vanadate on glucose tolerance,
insulin-mediated glucose disposal, glucose oxidation, glycolysis and
glycogen synthesis in healthy volunteers, IDDM and NIDDM subjects. This
will be a placebo-controlled trial to obtain preliminary information
regarding the short-term efficacy and safety of this trace element in
human subjects.
Effective start/end date9/30/939/29/98


  • Endocrinology, Diabetes and Metabolism


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