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Lipoprotein-associated oxidative stress: a new twist to the postprandial hypothesis.

Le NA - Int J Mol Sci (2014)

Bottom Line: This flux of dietary lipids is accompanied by concomitant increases in glucose, insulin and other meal-associated metabolites.The contribution of postprandial lipemia to the pathogenesis of atherosclerosis has been previously suggested by several lines of investigation.We have extended this hypothesis by demonstrating the acute generation of oxidative epitopes on plasma lipoproteins as well as transient changes in the oxidative susceptibility of plasma lipoproteins.

View Article: PubMed Central - PubMed

Affiliation: . Anh.Le@va.gov.

ABSTRACT
Oxidative stress is recognized as one of the primary processes underlying the initiation and progression of atherosclerotic vascular disease. Under physiological conditions, the balance between reactive oxygen species (ROS) generation and ROS scavenging is tightly controlled. As part of normal cellular metabolism, regulated oxidative stress is responsible for a variety of cellular responses. Excess generation of ROS that could not be compensated by antioxidant system has been suggested to be responsible for a number of pathological conditions. Due to their short biological half-lives, direct measurement of ROS is not available and surrogate measures are commonly used. Plasma lipoproteins, by virtue of their close interactions with endothelial cells in the vasculature and the susceptibility of their surface lipids to oxidative modification, are perfect biological sensors of oxidative stress in the arterial wall. In particular, with each consumed meal, triglyceride-rich lipoproteins, secreted by the intestine into the circulation, are responsible for the delivery of 20-40 grams of fat to the peripheral tissues. This flux of dietary lipids is accompanied by concomitant increases in glucose, insulin and other meal-associated metabolites. The contribution of postprandial lipemia to the pathogenesis of atherosclerosis has been previously suggested by several lines of investigation. We have extended this hypothesis by demonstrating the acute generation of oxidative epitopes on plasma lipoproteins as well as transient changes in the oxidative susceptibility of plasma lipoproteins.

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All lipoproteins isolated from fasting plasma are susceptible to oxidative modification in the presence of Cu2+ as a catalyst. (VLDL: Very-low density lipoproteins; LDL: Low-density lipoproteins; HDL: High-density lipoproteins; See [59] for details on the isolation procedure and incubation conditions).
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ijms-16-00401-f002: All lipoproteins isolated from fasting plasma are susceptible to oxidative modification in the presence of Cu2+ as a catalyst. (VLDL: Very-low density lipoproteins; LDL: Low-density lipoproteins; HDL: High-density lipoproteins; See [59] for details on the isolation procedure and incubation conditions).

Mentions: It should be noted that this oxidative process is not limited to plasma LDL but all plasma lipoproteins are susceptible to oxidative modification (Figure 2).


Lipoprotein-associated oxidative stress: a new twist to the postprandial hypothesis.

Le NA - Int J Mol Sci (2014)

All lipoproteins isolated from fasting plasma are susceptible to oxidative modification in the presence of Cu2+ as a catalyst. (VLDL: Very-low density lipoproteins; LDL: Low-density lipoproteins; HDL: High-density lipoproteins; See [59] for details on the isolation procedure and incubation conditions).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4307253&req=5

ijms-16-00401-f002: All lipoproteins isolated from fasting plasma are susceptible to oxidative modification in the presence of Cu2+ as a catalyst. (VLDL: Very-low density lipoproteins; LDL: Low-density lipoproteins; HDL: High-density lipoproteins; See [59] for details on the isolation procedure and incubation conditions).
Mentions: It should be noted that this oxidative process is not limited to plasma LDL but all plasma lipoproteins are susceptible to oxidative modification (Figure 2).

Bottom Line: This flux of dietary lipids is accompanied by concomitant increases in glucose, insulin and other meal-associated metabolites.The contribution of postprandial lipemia to the pathogenesis of atherosclerosis has been previously suggested by several lines of investigation.We have extended this hypothesis by demonstrating the acute generation of oxidative epitopes on plasma lipoproteins as well as transient changes in the oxidative susceptibility of plasma lipoproteins.

View Article: PubMed Central - PubMed

Affiliation: . Anh.Le@va.gov.

ABSTRACT
Oxidative stress is recognized as one of the primary processes underlying the initiation and progression of atherosclerotic vascular disease. Under physiological conditions, the balance between reactive oxygen species (ROS) generation and ROS scavenging is tightly controlled. As part of normal cellular metabolism, regulated oxidative stress is responsible for a variety of cellular responses. Excess generation of ROS that could not be compensated by antioxidant system has been suggested to be responsible for a number of pathological conditions. Due to their short biological half-lives, direct measurement of ROS is not available and surrogate measures are commonly used. Plasma lipoproteins, by virtue of their close interactions with endothelial cells in the vasculature and the susceptibility of their surface lipids to oxidative modification, are perfect biological sensors of oxidative stress in the arterial wall. In particular, with each consumed meal, triglyceride-rich lipoproteins, secreted by the intestine into the circulation, are responsible for the delivery of 20-40 grams of fat to the peripheral tissues. This flux of dietary lipids is accompanied by concomitant increases in glucose, insulin and other meal-associated metabolites. The contribution of postprandial lipemia to the pathogenesis of atherosclerosis has been previously suggested by several lines of investigation. We have extended this hypothesis by demonstrating the acute generation of oxidative epitopes on plasma lipoproteins as well as transient changes in the oxidative susceptibility of plasma lipoproteins.

Show MeSH
Related in: MedlinePlus