Citrus Polyphenol Hesperidin Stimulates Production of Nitric Oxide in Endothelial Cells while Improving Endothelial Function and Reducing Inflammatory Markers in Patients with Metabolic Syndrome

Context:Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological mechanisms of hesperetin actions are unknown.Objective:We tested whether hesperetin stimulates production of nitric oxide (NO) from vascular...

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Published inThe journal of clinical endocrinology and metabolism Vol. 96; no. 5; pp. E782 - E792
Main Authors Rizza, Stefano, Muniyappa, Ranganath, Iantorno, Micaela, Kim, Jeong-a, Chen, Hui, Pullikotil, Philomena, Senese, Nicoletta, Tesauro, Manfredi, Lauro, Davide, Cardillo, Carmine, Quon, Michael J.
Format Journal Article
LanguageEnglish
Published United States Oxford University Press 01.05.2011
Copyright by The Endocrine Society
Endocrine Society
Subjects
Adenylate Kinase - metabolism
AKT protein
Amyloid
Animals
C-reactive protein
Cattle
Cell Adhesion - drug effects
Cell adhesion molecules
Cell culture
Cells, Cultured
Clinical trials
Cross-Over Studies
Double-Blind Method
E-selectin
Endothelial cells
Endothelial Cells - drug effects
Endothelial Cells - metabolism
Endothelium
Endothelium, Vascular - physiology
Female
Flavonoids
Hesperidin
Hesperidin - pharmacology
Hot Topics in Translational Endocrinology
Humans
Hydrogen peroxide
Inflammation
Inflammation - metabolism
Kinases
Male
Metabolic syndrome
Metabolic Syndrome - metabolism
Metabolites
Middle Aged
Monocytes
Monocytes - drug effects
Nitric oxide
Nitric Oxide - biosynthesis
Nitric Oxide Synthase Type III - metabolism
Nitric-oxide synthase
Oncogene Protein v-akt - metabolism
Phosphorylation
Placebos
Signal Transduction - drug effects
Stimulation, Chemical
Tumor Necrosis Factor-alpha - antagonists & inhibitors
Tumor Necrosis Factor-alpha - pharmacology
Tumor necrosis factor-α
Vascular cell adhesion molecule 1
Vasodilation - physiology
Online AccessGet full text

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Abstract Context:Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological mechanisms of hesperetin actions are unknown.Objective:We tested whether hesperetin stimulates production of nitric oxide (NO) from vascular endothelium and evaluated endothelial function in subjects with metabolic syndrome on oral hesperidin therapy.Design, Setting, and Interventions:Cellular mechanisms of action of hesperetin were evaluated in bovine aortic endothelial cells (BAEC) in primary culture. A randomized, placebo-controlled, double-blind, crossover trial examined whether oral hesperidin administration (500 mg once daily for 3 wk) improves endothelial function in individuals with metabolic syndrome (n = 24).Main Outcome Measure:We measured the difference in brachial artery flow-mediated dilation between placebo and hesperidin treatment periods.Results:Treatment of BAEC with hesperetin acutely stimulated phosphorylation of Src, Akt, AMP kinase, and endothelial NO synthase to produce NO; this required generation of H2O2. Increased adhesion of monocytes to BAEC and expression of vascular cell adhesion molecule-1 in response to TNF-α treatment was reduced by pretreatment with hesperetin. In the clinical study, when compared with placebo, hesperidin treatment increased flow-mediated dilation (10.26 ± 1.19 vs. 7.78 ± 0.76%; P = 0.02) and reduced concentrations of circulating inflammatory biomarkers (high-sensitivity C-reactive protein, serum amyloid A protein, soluble E-selectin).Conclusions:Novel mechanisms for hesperetin action in endothelial cells inform effects of oral hesperidin treatment to improve endothelial dysfunction and reduce circulating markers of inflammation in our exploratory clinical trial. Hesperetin has vasculoprotective actions that may explain beneficial cardiovascular effects of citrus consumption.
AbstractList Signaling mechanisms were identified by which hesperetin stimulates endothelial nitric oxide production that informed this translational study, demonstrating that oral hesperidin treatment improves endothelial dysfunction.
CONTEXT:Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological mechanisms of hesperetin actions are unknown. OBJECTIVE:We tested whether hesperetin stimulates production of nitric oxide (NO) from vascular endothelium and evaluated endothelial function in subjects with metabolic syndrome on oral hesperidin therapy. DESIGN, SETTING, AND INTERVENTIONS:Cellular mechanisms of action of hesperetin were evaluated in bovine aortic endothelial cells (BAEC) in primary culture. A randomized, placebo-controlled, double-blind, crossover trial examined whether oral hesperidin administration (500 mg once daily for 3 wk) improves endothelial function in individuals with metabolic syndrome (n = 24). MAIN OUTCOME MEASURE:We measured the difference in brachial artery flow-mediated dilation between placebo and hesperidin treatment periods. RESULTS:Treatment of BAEC with hesperetin acutely stimulated phosphorylation of Src, Akt, AMP kinase, and endothelial NO synthase to produce NO; this required generation of H2O2. Increased adhesion of monocytes to BAEC and expression of vascular cell adhesion molecule-1 in response to TNF-α treatment was reduced by pretreatment with hesperetin. In the clinical study, when compared with placebo, hesperidin treatment increased flow-mediated dilation (10.26 ± 1.19 vs. 7.78 ± 0.76%; P = 0.02) and reduced concentrations of circulating inflammatory biomarkers (high-sensitivity C-reactive protein, serum amyloid A protein, soluble E-selectin). CONCLUSIONS:Novel mechanisms for hesperetin action in endothelial cells inform effects of oral hesperidin treatment to improve endothelial dysfunction and reduce circulating markers of inflammation in our exploratory clinical trial. Hesperetin has vasculoprotective actions that may explain beneficial cardiovascular effects of citrus consumption.
Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological mechanisms of hesperetin actions are unknown. We tested whether hesperetin stimulates production of nitric oxide (NO) from vascular endothelium and evaluated endothelial function in subjects with metabolic syndrome on oral hesperidin therapy. DESIGN, SETTING, AND INTERVENTIONS: Cellular mechanisms of action of hesperetin were evaluated in bovine aortic endothelial cells (BAEC) in primary culture. A randomized, placebo-controlled, double-blind, crossover trial examined whether oral hesperidin administration (500 mg once daily for 3 wk) improves endothelial function in individuals with metabolic syndrome (n = 24). We measured the difference in brachial artery flow-mediated dilation between placebo and hesperidin treatment periods. Treatment of BAEC with hesperetin acutely stimulated phosphorylation of Src, Akt, AMP kinase, and endothelial NO synthase to produce NO; this required generation of H(2)O(2). Increased adhesion of monocytes to BAEC and expression of vascular cell adhesion molecule-1 in response to TNF-α treatment was reduced by pretreatment with hesperetin. In the clinical study, when compared with placebo, hesperidin treatment increased flow-mediated dilation (10.26 ± 1.19 vs. 7.78 ± 0.76%; P = 0.02) and reduced concentrations of circulating inflammatory biomarkers (high-sensitivity C-reactive protein, serum amyloid A protein, soluble E-selectin). Novel mechanisms for hesperetin action in endothelial cells inform effects of oral hesperidin treatment to improve endothelial dysfunction and reduce circulating markers of inflammation in our exploratory clinical trial. Hesperetin has vasculoprotective actions that may explain beneficial cardiovascular effects of citrus consumption.
Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological mechanisms of hesperetin actions are unknown.CONTEXTHesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological mechanisms of hesperetin actions are unknown.We tested whether hesperetin stimulates production of nitric oxide (NO) from vascular endothelium and evaluated endothelial function in subjects with metabolic syndrome on oral hesperidin therapy. DESIGN, SETTING, AND INTERVENTIONS: Cellular mechanisms of action of hesperetin were evaluated in bovine aortic endothelial cells (BAEC) in primary culture. A randomized, placebo-controlled, double-blind, crossover trial examined whether oral hesperidin administration (500 mg once daily for 3 wk) improves endothelial function in individuals with metabolic syndrome (n = 24).OBJECTIVEWe tested whether hesperetin stimulates production of nitric oxide (NO) from vascular endothelium and evaluated endothelial function in subjects with metabolic syndrome on oral hesperidin therapy. DESIGN, SETTING, AND INTERVENTIONS: Cellular mechanisms of action of hesperetin were evaluated in bovine aortic endothelial cells (BAEC) in primary culture. A randomized, placebo-controlled, double-blind, crossover trial examined whether oral hesperidin administration (500 mg once daily for 3 wk) improves endothelial function in individuals with metabolic syndrome (n = 24).We measured the difference in brachial artery flow-mediated dilation between placebo and hesperidin treatment periods.MAIN OUTCOME MEASUREWe measured the difference in brachial artery flow-mediated dilation between placebo and hesperidin treatment periods.Treatment of BAEC with hesperetin acutely stimulated phosphorylation of Src, Akt, AMP kinase, and endothelial NO synthase to produce NO; this required generation of H(2)O(2). Increased adhesion of monocytes to BAEC and expression of vascular cell adhesion molecule-1 in response to TNF-α treatment was reduced by pretreatment with hesperetin. In the clinical study, when compared with placebo, hesperidin treatment increased flow-mediated dilation (10.26 ± 1.19 vs. 7.78 ± 0.76%; P = 0.02) and reduced concentrations of circulating inflammatory biomarkers (high-sensitivity C-reactive protein, serum amyloid A protein, soluble E-selectin).RESULTSTreatment of BAEC with hesperetin acutely stimulated phosphorylation of Src, Akt, AMP kinase, and endothelial NO synthase to produce NO; this required generation of H(2)O(2). Increased adhesion of monocytes to BAEC and expression of vascular cell adhesion molecule-1 in response to TNF-α treatment was reduced by pretreatment with hesperetin. In the clinical study, when compared with placebo, hesperidin treatment increased flow-mediated dilation (10.26 ± 1.19 vs. 7.78 ± 0.76%; P = 0.02) and reduced concentrations of circulating inflammatory biomarkers (high-sensitivity C-reactive protein, serum amyloid A protein, soluble E-selectin).Novel mechanisms for hesperetin action in endothelial cells inform effects of oral hesperidin treatment to improve endothelial dysfunction and reduce circulating markers of inflammation in our exploratory clinical trial. Hesperetin has vasculoprotective actions that may explain beneficial cardiovascular effects of citrus consumption.CONCLUSIONSNovel mechanisms for hesperetin action in endothelial cells inform effects of oral hesperidin treatment to improve endothelial dysfunction and reduce circulating markers of inflammation in our exploratory clinical trial. Hesperetin has vasculoprotective actions that may explain beneficial cardiovascular effects of citrus consumption.
Context:Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological mechanisms of hesperetin actions are unknown.Objective:We tested whether hesperetin stimulates production of nitric oxide (NO) from vascular endothelium and evaluated endothelial function in subjects with metabolic syndrome on oral hesperidin therapy.Design, Setting, and Interventions:Cellular mechanisms of action of hesperetin were evaluated in bovine aortic endothelial cells (BAEC) in primary culture. A randomized, placebo-controlled, double-blind, crossover trial examined whether oral hesperidin administration (500 mg once daily for 3 wk) improves endothelial function in individuals with metabolic syndrome (n = 24).Main Outcome Measure:We measured the difference in brachial artery flow-mediated dilation between placebo and hesperidin treatment periods.Results:Treatment of BAEC with hesperetin acutely stimulated phosphorylation of Src, Akt, AMP kinase, and endothelial NO synthase to produce NO; this required generation of H2O2. Increased adhesion of monocytes to BAEC and expression of vascular cell adhesion molecule-1 in response to TNF-α treatment was reduced by pretreatment with hesperetin. In the clinical study, when compared with placebo, hesperidin treatment increased flow-mediated dilation (10.26 ± 1.19 vs. 7.78 ± 0.76%; P = 0.02) and reduced concentrations of circulating inflammatory biomarkers (high-sensitivity C-reactive protein, serum amyloid A protein, soluble E-selectin).Conclusions:Novel mechanisms for hesperetin action in endothelial cells inform effects of oral hesperidin treatment to improve endothelial dysfunction and reduce circulating markers of inflammation in our exploratory clinical trial. Hesperetin has vasculoprotective actions that may explain beneficial cardiovascular effects of citrus consumption.
Author Iantorno, Micaela
Kim, Jeong-a
Senese, Nicoletta
Cardillo, Carmine
Rizza, Stefano
Chen, Hui
Pullikotil, Philomena
Quon, Michael J.
Muniyappa, Ranganath
Lauro, Davide
Tesauro, Manfredi
AuthorAffiliation Diabetes Unit (R.M., M.I., H.C., P.P., M.J.Q.), National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892; Department of Internal Medicine (S.R., N.S., M.T., D.L.), University of Rome “Tor Vergata”, 00133 Rome, Italy; Department of Internal Medicine (C.C.), Catholic University “Sacro Cuore”, 00168 Rome, Italy; and Department of Medicine (J.K.), Division of Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama 39294
AuthorAffiliation_xml – name: Diabetes Unit (R.M., M.I., H.C., P.P., M.J.Q.), National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892; Department of Internal Medicine (S.R., N.S., M.T., D.L.), University of Rome “Tor Vergata”, 00133 Rome, Italy; Department of Internal Medicine (C.C.), Catholic University “Sacro Cuore”, 00168 Rome, Italy; and Department of Medicine (J.K.), Division of Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama 39294
Author_xml – sequence: 1
  givenname: Stefano
  surname: Rizza
  fullname: Rizza, Stefano
  organization: 2Department of Internal Medicine (S.R., N.S., M.T., D.L.), University of Rome “Tor Vergata”, 00133 Rome, Italy
– sequence: 2
  givenname: Ranganath
  surname: Muniyappa
  fullname: Muniyappa, Ranganath
  organization: 1Diabetes Unit (R.M., M.I., H.C., P.P., M.J.Q.), National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892
– sequence: 3
  givenname: Micaela
  surname: Iantorno
  fullname: Iantorno, Micaela
  organization: 1Diabetes Unit (R.M., M.I., H.C., P.P., M.J.Q.), National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892
– sequence: 4
  givenname: Jeong-a
  surname: Kim
  fullname: Kim, Jeong-a
  organization: 4Department of Medicine (J.K.), Division of Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama 39294
– sequence: 5
  givenname: Hui
  surname: Chen
  fullname: Chen, Hui
  organization: 1Diabetes Unit (R.M., M.I., H.C., P.P., M.J.Q.), National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892
– sequence: 6
  givenname: Philomena
  surname: Pullikotil
  fullname: Pullikotil, Philomena
  organization: 1Diabetes Unit (R.M., M.I., H.C., P.P., M.J.Q.), National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892
– sequence: 7
  givenname: Nicoletta
  surname: Senese
  fullname: Senese, Nicoletta
  organization: 2Department of Internal Medicine (S.R., N.S., M.T., D.L.), University of Rome “Tor Vergata”, 00133 Rome, Italy
– sequence: 8
  givenname: Manfredi
  surname: Tesauro
  fullname: Tesauro, Manfredi
  organization: 2Department of Internal Medicine (S.R., N.S., M.T., D.L.), University of Rome “Tor Vergata”, 00133 Rome, Italy
– sequence: 9
  givenname: Davide
  surname: Lauro
  fullname: Lauro, Davide
  organization: 2Department of Internal Medicine (S.R., N.S., M.T., D.L.), University of Rome “Tor Vergata”, 00133 Rome, Italy
– sequence: 10
  givenname: Carmine
  surname: Cardillo
  fullname: Cardillo, Carmine
  organization: 3Department of Internal Medicine (C.C.), Catholic University “Sacro Cuore”, 00168 Rome, Italy
– sequence: 11
  givenname: Michael J.
  surname: Quon
  fullname: Quon, Michael J.
  email: quonm@medicine.umaryland.edu
  organization: 1Diabetes Unit (R.M., M.I., H.C., P.P., M.J.Q.), National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892
BackLink https://www.ncbi.nlm.nih.gov/pubmed/21346065$$D View this record in MEDLINE/PubMed
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Snippet Context:Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological...
CONTEXT:Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological...
Hesperidin, a citrus flavonoid, and its metabolite hesperetin may have vascular actions relevant to their health benefits. Molecular and physiological...
Signaling mechanisms were identified by which hesperetin stimulates endothelial nitric oxide production that informed this translational study, demonstrating...
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SubjectTerms Adenylate Kinase - metabolism
AKT protein
Amyloid
Animals
C-reactive protein
Cattle
Cell Adhesion - drug effects
Cell adhesion molecules
Cell culture
Cells, Cultured
Clinical trials
Cross-Over Studies
Double-Blind Method
E-selectin
Endothelial cells
Endothelial Cells - drug effects
Endothelial Cells - metabolism
Endothelium
Endothelium, Vascular - physiology
Female
Flavonoids
Hesperidin
Hesperidin - pharmacology
Hot Topics in Translational Endocrinology
Humans
Hydrogen peroxide
Inflammation
Inflammation - metabolism
Kinases
Male
Metabolic syndrome
Metabolic Syndrome - metabolism
Metabolites
Middle Aged
Monocytes
Monocytes - drug effects
Nitric oxide
Nitric Oxide - biosynthesis
Nitric Oxide Synthase Type III - metabolism
Nitric-oxide synthase
Oncogene Protein v-akt - metabolism
Phosphorylation
Placebos
Signal Transduction - drug effects
Stimulation, Chemical
Tumor Necrosis Factor-alpha - antagonists & inhibitors
Tumor Necrosis Factor-alpha - pharmacology
Tumor necrosis factor-α
Vascular cell adhesion molecule 1
Vasodilation - physiology
Title Citrus Polyphenol Hesperidin Stimulates Production of Nitric Oxide in Endothelial Cells while Improving Endothelial Function and Reducing Inflammatory Markers in Patients with Metabolic Syndrome
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https://pubmed.ncbi.nlm.nih.gov/PMC3085197
Volume 96
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