A new chromanone isolated from Portulaca oleracea L. increases glucose uptake by stimulating GLUT4 translocation to the plasma membrane in 3T3-L1 adipocytes

Int J Biol Macromol. 2019 Feb 15:123:26-34. doi: 10.1016/j.ijbiomac.2018.10.206. Epub 2018 Oct 30.

Abstract

Three homoisoflavonoids and one dimethoxychalcone from Portulaca oleracea L. were isolated using bioassay-guided fractionation and HPLC. Among the compounds 1-4, (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone (compound 3) had the most effect on glucose uptake in the adipocytes. We investigated how (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone contributed to increase glucose uptake in 3T3-L1 adipocytes. Levels of the glucose transporters GLUT-4, as well as glucose uptake, and key proteins of the insulin pathway, namely PI3K/AKT and AMPK pathway are analyzed using glucose uptake assay and western blot analysis. Our results show that (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone significantly increased glucose uptake by stimulating translocation of GLUT4 to the plasma membrane in 3T3-L1 adipocytes. High levels of expression of GLUT4 in the plasma membrane resulted from IRS-1 phosphorylation, PI3K activation, Akt phosphorylation and phosphorylation of AMPK, resulting in increased glucose uptake by the cells. The increase in glucose uptake due to (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone was significantly inhibited by the PI3K inhibitor and the AMPK inhibitor in 3T3-L1 adipocytes. These findings suggest that (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone may increase glucose uptake by stimulating GLUT4 translocation to the plasma membrane via activating the PI3K/Akt and AMPK pathways in 3T3-L1 adipocytes.

Keywords: 3T3-L1 adipocytes; AMPK; Diabetes; Glucose uptake; Homoisoflavonoid; PI3K/Akt.

MeSH terms

  • 3T3-L1 Cells
  • AMP-Activated Protein Kinases / metabolism
  • Adipocytes / drug effects*
  • Adipocytes / metabolism
  • Animals
  • Carbohydrate Metabolism / drug effects
  • Cell Line
  • Cell Membrane / drug effects*
  • Glucose / metabolism*
  • Glucose Transporter Type 4 / metabolism*
  • Hypoglycemic Agents / pharmacology
  • Insulin / metabolism
  • Mice
  • Phosphatidylinositol 3-Kinases / metabolism
  • Phosphorylation / drug effects
  • Plant Extracts / pharmacology*
  • Portulaca / chemistry*
  • Protein Transport / drug effects*
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects

Substances

  • Glucose Transporter Type 4
  • Hypoglycemic Agents
  • Insulin
  • Plant Extracts
  • Slc2a4 protein, mouse
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • AMP-Activated Protein Kinases
  • Glucose