Nandinine, a Derivative of Berberine, Inhibits Inflammation and Reduces Insulin Resistance in Adipocytes via Regulation of AMP-Kinase Activity

Planta Med. 2017 Feb;83(3-04):203-209. doi: 10.1055/s-0042-110576. Epub 2016 Jul 27.

Abstract

Nandinine is a derivative of berberine that has high efficacy for treating cardiovascular diseases. This study investigated the effects of berberine and nandinine on the regulation of insulin sensitivity in adipocytes. Through treatment with macrophage-derived conditioned medium in 3T3-L1 adipocytes, dysregulation of adipokine production and activation of the IκB kinase β/nuclear factor-kappa B pathway was induced. However, these phenomena were effectively reversed by berberine, nandinine, and salicylate pretreatments. Furthermore, both berberine and nandinine inhibited serine phosphorylation of insulin receptor substrate-1 induced by IκB kinase β and increased tyrosine phosphorylation of insulin receptor substrate-1 to activate the PI3K/Akt pathway, which finally led to insulin-mediated glucose uptake. In addition, berberine and nandinine significantly increased AMP-activated protein kinase activity, thereby contributing to their anti-inflammatory effect by inhibiting IκB kinase β activation. Finally, in vivo studies demonstrated that both berberine (100 or 200 mg/kg) and nandinine (100 or 200 mg/kg) effectively ameliorated glucose intolerance and induced the insulin sensitivity index in mice. In conclusion, berberine and nandinine attenuated insulin resistance in adipocytes by inhibiting inflammation in an AMP-activated protein kinase-dependent manner. Berberine and nandinine may be used as dietary supplements and nandinine is a new candidate for obesity treatment.

MeSH terms

  • 3T3-L1 Cells
  • AMP-Activated Protein Kinases / metabolism
  • Adenylate Kinase / metabolism*
  • Adipocytes / drug effects*
  • Adipocytes / enzymology
  • Adipocytes / metabolism
  • Animals
  • Berberine Alkaloids / chemistry
  • Berberine Alkaloids / pharmacology*
  • Biological Transport / drug effects
  • Glucose / metabolism
  • I-kappa B Kinase / metabolism
  • Inflammation / drug therapy*
  • Inflammation / metabolism
  • Insulin / metabolism
  • Insulin Receptor Substrate Proteins / metabolism
  • Insulin Resistance*
  • Interleukin-6 / biosynthesis
  • Macrophages / drug effects
  • Macrophages / enzymology
  • Macrophages / metabolism
  • Male
  • Mice
  • Mice, Inbred ICR
  • NF-kappaB-Inducing Kinase
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • Salicylates / pharmacology
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Berberine Alkaloids
  • Insulin
  • Insulin Receptor Substrate Proteins
  • Interleukin-6
  • Salicylates
  • Tumor Necrosis Factor-alpha
  • interleukin-6, mouse
  • Protein Serine-Threonine Kinases
  • I-kappa B Kinase
  • AMP-Activated Protein Kinases
  • Adenylate Kinase
  • Glucose