Multidrug and toxic compound extrusion protein-1 (MATE1/SLC47A1) is a novel flavonoid transporter

Ji Hae Lee, Jung Eun Lee, Yeojin Kim, Hojoung Lee, Hee Jin Jun, Sung-Joon Lee

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Dietary flavonoids have various biological functions. However, their cellular transport mechanisms are largely unknown. We have determined that the multidrug and toxic compound extrusion transporter-1 (MATE1) is a membrane transporter for flavonoids and has a high affinity for quercetin. HEK293T cells overexpressing MATE1 exhibited increased intracellular quercetin accumulation. This effect disappeared in the presence of a MATE1 inhibitor and after MATE1 gene knockdown. HepG2 cells expressed MATE1 significantly, with the uptake quercetin of which was dramatically reduced with MATE1 inhibition. On the basis of immunofluorescence analysis, MATE1 was highly expressed in peroxisomes and the endoplasmic reticulum (ER) as well as in plasma membranes in the liver and intestine, which suggests potential accumulation of quercetin in peroxisomes and the ER in these tissues. Fluorescent microscopic analysis confirmed selective accumulation of qurcetin in peroxisome. The effects of quercetin on cellular lipid reduction and glucose uptake were exaggerated with MATE1 overexpression. In conclusion, MATE1 is a membrane transporter for quercetin; its overexpression enhances the hypolipidemic activity of quercetin and cellular glucose transport. Considering the low bioavailability of quercetin, appropriate regulation of MATE1 expression may optimize cellular quercetin concentrations and promote health benefits.

Original languageEnglish
Pages (from-to)9690-9698
Number of pages9
JournalJournal of Agricultural and Food Chemistry
Volume62
Issue number40
DOIs
Publication statusPublished - 2014 Oct 8

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Keywords

  • flavonoid transporter
  • lipid metabolism
  • multidrug and toxic compound extrusion transporter-1
  • quercetin

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Chemistry(all)
  • Medicine(all)

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