Berberine improves insulin resistance in cardiomyocytes via activation of 5′-adenosine monophosphate-activated protein kinase

Abstract

ObjectiveInsulin resistance plays an important role in the pathogenesis of diabetic cardiomyopathy. Berberine (BBR) is a plant alkaloid which promotes hypoglycemia via increasing insulin sensitivity in peripheral tissues. Little is known of BBR’s role in regulating glucose metabolism in heart. Materials/methodsWe examined the effect and mechanism of BBR on glucose consumption and glucose uptake in insulin sensitive or insulin resistant rat H9c2 cardiomyocyte cells. H9c2 myoblast cells were differentiated into cardiomyocytes and incubated with insulin for 24h to induce insulin resistance. ResultsBBR-treatment of H9c2 cells increased glucose consumption and glucose uptake compared to controls. In addition, BBR-treatment attenuated the reduction in glucose consumption and glucose uptake in insulin resistant H9c2 cells. Compound C, an inhibitor of AMP-activated protein kinase (AMPK), abolished the enhancement of glucose consumption and glucose uptake mediated by BBR in both insulin sensitive and insulin resistant H9c2 cells compared to controls. ConclusionBBR significantly increased AMPK activity, but had little effect on the activity of protein kinase B (AKT) in insulin resistant H9c2 cells, suggesting that berberine improves insulin resistance in H9c2 cardiomyocytes at least in part via stimulation of AMPK activity.