Methionine‐induced hyperhomocysteinemia impairs the antioxidant ability of high‐density lipoproteins without reducing in vivo macrophage‐specific reverse cholesterol transport. Issue 10 (10th June 2013)
- Record Type:
- Journal Article
- Title:
- Methionine‐induced hyperhomocysteinemia impairs the antioxidant ability of high‐density lipoproteins without reducing in vivo macrophage‐specific reverse cholesterol transport. Issue 10 (10th June 2013)
- Main Title:
- Methionine‐induced hyperhomocysteinemia impairs the antioxidant ability of high‐density lipoproteins without reducing in vivo macrophage‐specific reverse cholesterol transport
- Authors:
- Julve, Josep
Escolà‐Gil, Joan C.
Rodríguez‐Millán, Elisabeth
Martín‐Campos, Jesús M.
Jauhiainen, Matti
Quesada, Helena
Rentería‐Obregón, Ivy M.
Osada, Jesús
Sánchez‐Quesada, José L.
Blanco‐Vaca, Francisco - Abstract:
- <abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2003-sec-0010" sec-type="section"> <title>Scope</title> <p>High plasma homocysteine concentrations have been associated with increased risk of cardiovascular disease both in humans and experimental animal models, whereas plasma HDL‐cholesterol concentration is inversely correlated with such disorders. This work aimed to study the impact of methionine‐induced hyperhomocysteinemia (HHcy) on two major antiatherogenic functions of HDL, namely their capacity to prevent LDL oxidation and induce in vivo macrophage‐specific reverse cholesterol transport.</p> </sec> <sec id="mnfr2003-sec-0020" sec-type="section"> <title>Methods and results</title> <p>Methionine‐induced HHcy in mice resulted in an approximately 20% decreased concentration of HDL‐cholesterol and HDL main protein component, apolipoprotein A‐I. The HDL potential to resist oxidation as well as to prevent LDL oxidative modification was impaired in hyperhomocysteinemic mice. Activities of paraoxonase‐1 and platelet activation factor acetylhydrolase, two of the main HDL‐associated enzymes with antioxidant activity, were reduced. The ability of HDL to efflux cholesterol from macrophages was decreased in hyperhomocysteinemic mice; however, the in vivo macrophage‐specific reverse cholesterol transport measured as the output of labeled cholesterol into feces did not significantly differ between groups.</p> </sec> <sec<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2003-sec-0010" sec-type="section"> <title>Scope</title> <p>High plasma homocysteine concentrations have been associated with increased risk of cardiovascular disease both in humans and experimental animal models, whereas plasma HDL‐cholesterol concentration is inversely correlated with such disorders. This work aimed to study the impact of methionine‐induced hyperhomocysteinemia (HHcy) on two major antiatherogenic functions of HDL, namely their capacity to prevent LDL oxidation and induce in vivo macrophage‐specific reverse cholesterol transport.</p> </sec> <sec id="mnfr2003-sec-0020" sec-type="section"> <title>Methods and results</title> <p>Methionine‐induced HHcy in mice resulted in an approximately 20% decreased concentration of HDL‐cholesterol and HDL main protein component, apolipoprotein A‐I. The HDL potential to resist oxidation as well as to prevent LDL oxidative modification was impaired in hyperhomocysteinemic mice. Activities of paraoxonase‐1 and platelet activation factor acetylhydrolase, two of the main HDL‐associated enzymes with antioxidant activity, were reduced. The ability of HDL to efflux cholesterol from macrophages was decreased in hyperhomocysteinemic mice; however, the in vivo macrophage‐specific reverse cholesterol transport measured as the output of labeled cholesterol into feces did not significantly differ between groups.</p> </sec> <sec id="mnfr2003-sec-0030" sec-type="section"> <title>Conclusion</title> <p>Our data indicate that the HDL from methionine‐induced hyperhomocysteinemic mice was more prone to oxidation and displayed lower capacity to protect LDL against oxidative modification than that of control mice, highlighting a mechanism by which a diet‐induced HHcy may facilitate progression of atherosclerosis.</p> </sec> </abstract> … (more)
- Is Part Of:
- Molecular nutrition & food research. Volume 57:Issue 10(2013:Oct.)
- Journal:
- Molecular nutrition & food research
- Issue:
- Volume 57:Issue 10(2013:Oct.)
- Issue Display:
- Volume 57, Issue 10 (2013)
- Year:
- 2013
- Volume:
- 57
- Issue:
- 10
- Issue Sort Value:
- 2013-0057-0010-0000
- Page Start:
- 1814
- Page End:
- 1824
- Publication Date:
- 2013-06-10
- Subjects:
- Food -- Biotechnology -- Periodicals
Food -- Microbiology -- Periodicals
Nutrition -- Periodicals
Food -- Toxicology -- Periodicals
Nutrition -- Periodicals
Food Microbiology -- Periodicals
Food Technology -- Periodicals
Molecular Biology -- Periodicals
664.0705 - Journal URLs:
- http://onlinelibrary.wiley.com/ ↗
- DOI:
- 10.1002/mnfr.201300133 ↗
- Languages:
- English
- ISSNs:
- 1613-4125
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 5900.817992
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 3804.xml