Mechanisms of Action
Corosolic acid is suggested to induce GLUT4 translocation [9,10]. Translocation of more GLUT4 glucose transporters to the cell surface means increased insulin action [11]. Disrupted GLUT4 gene has been shown to cause insulin resistance in skeletal muscles as well as diabetes [12]. Corosolic acid also works as “insulin sensitizer” by inhibiting enzymatic activities of several diabetes-related non-receptor protein tyrosine phosphatases (such as PTP1B) which indirectly enhances insulin receptor B phosphorylation [9]. Inhibition of protein tyrosine phosphatase 1B is an attractive target for treatment of diabetes and obesity [13,14]. Corosolic acid also promotes glycolysis [5] and suppresses gluconeogenesis (via increased production of fructose-2,6-bisphosphate) [15].
Cortisol Regulation
Corosolic acid is a potent and selective inhibitor of the enzyme (11-beta hydroxysteroid dehydrogenase type 1) that converts inactive cortisone to active cortisol [18]. Therefore, corosolic acid may prevent excessive cortisol production.
Corosolic acid is suggested to induce GLUT4 translocation [9,10]. Translocation of more GLUT4 glucose transporters to the cell surface means increased insulin action [11]. Disrupted GLUT4 gene has been shown to cause insulin resistance in skeletal muscles as well as diabetes [12]. Corosolic acid also works as “insulin sensitizer” by inhibiting enzymatic activities of several diabetes-related non-receptor protein tyrosine phosphatases (such as PTP1B) which indirectly enhances insulin receptor B phosphorylation [9]. Inhibition of protein tyrosine phosphatase 1B is an attractive target for treatment of diabetes and obesity [13,14]. Corosolic acid also promotes glycolysis [5] and suppresses gluconeogenesis (via increased production of fructose-2,6-bisphosphate) [15].
Cortisol Regulation
Corosolic acid is a potent and selective inhibitor of the enzyme (11-beta hydroxysteroid dehydrogenase type 1) that converts inactive cortisone to active cortisol [18]. Therefore, corosolic acid may prevent excessive cortisol production.
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