title: Berberine improves insulin resistance in cardiomyocytes via activation of 5'-adenosine monophosphate-activated protein kinase.
abstract: OBJECTIVE
  Insulin 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.
  
  
  METHODS
  We 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.
  
  
  RESULTS
  BBR-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.
  
  
  CONCLUSIONS
  BBR 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.
authors.affiliation: Department of Pharmacology, Norman Bethune Medical College, Jilin University, Changchun 130021, China.
authors.forename: Wenguang
authors.initials: W
authors.lastname: Chang
authors.forename: Ming
authors.initials: M
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Zhaojie
authors.initials: Z
authors.lastname: Meng
authors.forename: Shengnan
authors.initials: S
authors.lastname: Wei
authors.forename: Hongwei
authors.initials: H
authors.lastname: Du
authors.forename: Li
authors.initials: L
authors.lastname: Chen
authors.forename: Grant M
authors.initials: GM
authors.lastname: Hatch
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000502:physiology*; D000620:Aminoimidazole Carboxamide / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001562:Benzimidazoles; D001599:Berberine / Q000494:pharmacology*; D015153:Blotting, Western; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D005456:Fluorescent Dyes; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007333:Insulin Resistance / Q000502:physiology*; D008856:Microscopy, Fluorescence; D032383:Myocytes, Cardiac / Q000187:drug effects*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D012265:Ribonucleotides / Q000494:pharmacology
chemical_list: D001562:Benzimidazoles; D005456:Fluorescent Dyes; D007004:Hypoglycemic Agents; D047428:Protein Kinase Inhibitors; D012265:Ribonucleotides; D001599:Berberine; D000620:Aminoimidazole Carboxamide; D051057:Proto-Oncogene Proteins c-akt; D055372:AMP-Activated Protein Kinases; C031143:AICA ribonucleotide; D005947:Glucose; C017807:bisbenzimide ethoxide trihydrochloride
keywords: 5′-adenosine monophosphate-activated protein kinase; AKT; AMP; AMPK; BBR; Berberine; DCM; GLUT-4; Glucose consumption; H9c2; IRS-1; Insulin resistance; PBS; adenosine monophosphate; berberine; diabetic cardiomyopathy; glucose transporter-4; insulin receptor substrate-1; phosphate buffered solution; protein kinase B(PKB)