Low-Density-Lipoprotein (LDL)-bound flavonoids increase the resistance of LDL to oxidation and glycation under pathophysiological concentrations of glucose in vitro

Chi H. Wu, Jer A. Lin, Wen Ching Hsieh, Gow Chin Yen

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The higher susceptibility of low-density lipoprotein (LDL) to oxidation and glycation in diabetes has been shown to be related to poor glycemic control. The aim of this study was to determine whether LDL-bound flavonoids attenuate high-glucose (HG)-mediated LDL oxidation and glycation. For this purpose, human plasma was preincubated with individual flavonoids for 3 h, followed by sequential ultracentrifugation and extensive dialysis to remove unbound flavonoid samples. Enriched LDL was subsequently isolated and challenged for its resistance to oxidation and glycation. Results showed that glucose (5-30 mM) dose-dependently accelerates copper (Cu2+)-mediated LDL oxidatlve modification. The enrichment of flavonoids such as luteolin, naringenln, and kaempferol significantly increased the resistance of LDL to oxidation and prevented endogenous α-tocopherol consumption caused by HG/Cu2+ (p <0.05). The long-term glycation of LDL, which was measured by advanced glycation endproducts (AGEs)-related fluorescence and boronate affinity chromatography, was found to be inhibited by LDL-bound flavonoids in the following order: rutin > luteolin > quercetin > kaempferol > naringenin > catechin ≈ EC > naringin. Moreover, a solid-phase extraction system with HPLC-diode array detection provided evidence that flavonoids were bound to LDL particles to a certain extent concurrently facilitating the lipoprotein antioxidant and antiglycation activities. In conclusion, this study supports the hypothesis that HG promoted oxidative and glycative modifications of LDL. This is the first study to show that the introduction of flavonoids into LDL particles protects the lipoprotein against glycotoxin-medlated adverse effects.

Original languageEnglish
Pages (from-to)5058-5064
Number of pages7
JournalJournal of Agricultural and Food Chemistry
Volume57
Issue number11
DOIs
Publication statusPublished - Jun 10 2009
Externally publishedYes

Fingerprint

glycation
low density lipoprotein
LDL Lipoproteins
Flavonoids
flavonoids
oxidation
Glucose
Oxidation
glucose
Luteolin
luteolin
kaempferol
lipoproteins
Lipoproteins
Plasma (human)
naringin
In Vitro Techniques
glycemic control
naringenin
Tocopherols

Keywords

  • Advanced glycation endproducts
  • Binging
  • Flavonoids
  • Glucose
  • Glycation
  • LDL
  • Oxidation
  • Tocopherol

ASJC Scopus subject areas

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

Cite this

Low-Density-Lipoprotein (LDL)-bound flavonoids increase the resistance of LDL to oxidation and glycation under pathophysiological concentrations of glucose in vitro. / Wu, Chi H.; Lin, Jer A.; Hsieh, Wen Ching; Yen, Gow Chin.

In: Journal of Agricultural and Food Chemistry, Vol. 57, No. 11, 10.06.2009, p. 5058-5064.

Research output: Contribution to journalArticle

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T1 - Low-Density-Lipoprotein (LDL)-bound flavonoids increase the resistance of LDL to oxidation and glycation under pathophysiological concentrations of glucose in vitro

AU - Wu, Chi H.

AU - Lin, Jer A.

AU - Hsieh, Wen Ching

AU - Yen, Gow Chin

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N2 - The higher susceptibility of low-density lipoprotein (LDL) to oxidation and glycation in diabetes has been shown to be related to poor glycemic control. The aim of this study was to determine whether LDL-bound flavonoids attenuate high-glucose (HG)-mediated LDL oxidation and glycation. For this purpose, human plasma was preincubated with individual flavonoids for 3 h, followed by sequential ultracentrifugation and extensive dialysis to remove unbound flavonoid samples. Enriched LDL was subsequently isolated and challenged for its resistance to oxidation and glycation. Results showed that glucose (5-30 mM) dose-dependently accelerates copper (Cu2+)-mediated LDL oxidatlve modification. The enrichment of flavonoids such as luteolin, naringenln, and kaempferol significantly increased the resistance of LDL to oxidation and prevented endogenous α-tocopherol consumption caused by HG/Cu2+ (p <0.05). The long-term glycation of LDL, which was measured by advanced glycation endproducts (AGEs)-related fluorescence and boronate affinity chromatography, was found to be inhibited by LDL-bound flavonoids in the following order: rutin > luteolin > quercetin > kaempferol > naringenin > catechin ≈ EC > naringin. Moreover, a solid-phase extraction system with HPLC-diode array detection provided evidence that flavonoids were bound to LDL particles to a certain extent concurrently facilitating the lipoprotein antioxidant and antiglycation activities. In conclusion, this study supports the hypothesis that HG promoted oxidative and glycative modifications of LDL. This is the first study to show that the introduction of flavonoids into LDL particles protects the lipoprotein against glycotoxin-medlated adverse effects.

AB - The higher susceptibility of low-density lipoprotein (LDL) to oxidation and glycation in diabetes has been shown to be related to poor glycemic control. The aim of this study was to determine whether LDL-bound flavonoids attenuate high-glucose (HG)-mediated LDL oxidation and glycation. For this purpose, human plasma was preincubated with individual flavonoids for 3 h, followed by sequential ultracentrifugation and extensive dialysis to remove unbound flavonoid samples. Enriched LDL was subsequently isolated and challenged for its resistance to oxidation and glycation. Results showed that glucose (5-30 mM) dose-dependently accelerates copper (Cu2+)-mediated LDL oxidatlve modification. The enrichment of flavonoids such as luteolin, naringenln, and kaempferol significantly increased the resistance of LDL to oxidation and prevented endogenous α-tocopherol consumption caused by HG/Cu2+ (p <0.05). The long-term glycation of LDL, which was measured by advanced glycation endproducts (AGEs)-related fluorescence and boronate affinity chromatography, was found to be inhibited by LDL-bound flavonoids in the following order: rutin > luteolin > quercetin > kaempferol > naringenin > catechin ≈ EC > naringin. Moreover, a solid-phase extraction system with HPLC-diode array detection provided evidence that flavonoids were bound to LDL particles to a certain extent concurrently facilitating the lipoprotein antioxidant and antiglycation activities. In conclusion, this study supports the hypothesis that HG promoted oxidative and glycative modifications of LDL. This is the first study to show that the introduction of flavonoids into LDL particles protects the lipoprotein against glycotoxin-medlated adverse effects.

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