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Metabolites of polyphenols preserve indices of endothelial cell nitric oxide bioavailability under glucotoxic conditions (372.6)
Author(s) -
Qian Ying,
Panneerseelan Leenalitha,
Babu P.V.A.,
Symons J.,
Jalili Thunder
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.372.6
Subject(s) - enos , protein kinase b , nitric oxide , resveratrol , insulin , chemistry , bioavailability , quercetin , medicine , endocrinology , polyphenol , oxidative stress , glucose uptake , nitric oxide synthase , pharmacology , biochemistry , apoptosis , antioxidant , organic chemistry
We hypothesized that biological metabolites of quercetin, resveratrol, and grape seed extract previously identified in human plasma can prevent impairment of nitric oxide (NO) bioavailability due to glucotoxic conditions (e.g. Type 1 or 2 diabetes). Human aortic endothelial cells were treated for 24 h with 2μΜ Quercetin‐3‐O‐glucoronide, 5μΜ Piceatannol, or 1μΜ 3‐Hydroproponoic acid. Cells were next exposed to normal (5mM) or high (25mM) glucose for 48h, then treated with insulin (100nM, 10 min) to stimulate NO production. In the absence of polyphenols, insulin stimulation increased (P<0.05) indices of NO production, phosphorylated to total Akt (p‐Akt Ser473 :Akt), and endothelial nitric oxide synthase (p‐eNOS ser1177 :eNOS) in cells grown in 5mM but not 25mM glucose. Pretreatment of cells with polyphenol metabolites prior to 25mM glucose exposure preserved insulin stimulated increases (P<0.05) in NO, p‐Akt Ser473 :Akt and p‐eNOS ser1177 :eNOS. These effects may be secondary to oxidative stress as elevations (P<0.05) in reactive oxygen and nitrogen species in cells treated with 25mM glucose were completely prevented by all polyphenol metabolites. These data indicate that biological metabolites of quercetin, resveratrol, and grape seed extract protected against gluocotoxic impairment of insulin dependent NO bioavailability, and preserved the insulin ‐ Akt ‐ eNOS signaling axis.