Fructose Ingestion Enhances Atherosclerosis and Deposition of Advanced Glycated End-products in Cholesterol-fed Rabbits

Tokita, Yoshihisa; Hirayama, Yoshitake; Sekikawa, Akihiro; Kotake, Hidetoshi; Toyota, Takayoshi; Miyazawa, Teruo; Sawai, Takashi; Oikawa, Shinichi

doi:10.5551/jat.12.260

Cited by 30 publications

(19 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oxidative lipid modifications play important roles in the pathogenesis of atherosclerosis (1)(2)(3)(4). Among oxidatively modified lipids, phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), was observed to be accumulated in arterial walls and blood plasma in atherosclerotic rabbits (5). PCOOH was also identified in human atherosclerotic lesions (6,7).…”

mentioning

confidence: 98%

Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1

Asai

Okajima

Nakagawa

et al. 2009

Journal of Lipid Research

Self Cite

View full text Add to dashboard Cite

The accumulation of phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), in blood plasma and tissues has been observed in various pathological conditions, including atherosclerosis. However, the biological roles of PCOOH in these conditions remain unknown. To estimate the atherogenicity of PCOOH, we evaluated the effect of PCOOH on THP-1 monocytic cell adherence to immobilized vascular endothelial cell adhesion molecules. THP-1 cell adhesion to intracellular adhesion molecule-1 (ICAM-1) was dosedependently increased by addition of PCOOH. Phosphatidylcholine hydroxide (a hydroxyl analog of PCOOH) also induced THP-1 cell adhesion to ICAM-1, whereas nonoxidized PC, sn-2 truncated PCs, and other hydroperoxide compounds did not affect the adhesion. In the PCOOH-treated cells, obvious protruding F-actin-rich membrane structures were formed, and lymphocyte function-associated antigen-1 (LFA-1) was localized to the protruding structures. Cytochalasin D, an actin polymerization inhibitor, suppressed the PCOOH-induced cell adhesion to ICAM-1 and the membrane protrusions. These results indicate that PCOOH evokes LFA-1-mediated cell adhesion to ICAM-1 via actin cytoskeletal organization, and the mechanism may participate in monocyte adherence to the arterial wall in the initiation of atherosclerosis.-Asai, A., F. Okajima, K. Nakagawa, D. Ibusuki, K. Tanimura, Y. Nakajima, M. Nagao, M. Sudo, T. Harada, T. Miyazawa, and S. Oikawa. Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1. J. Lipid Res. 2009. 50: 957-965. Supplementary key words lipid oxidationOxidative lipid modifications play important roles in the pathogenesis of atherosclerosis (1-4). Among oxidatively modified lipids, phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), was observed to be accumulated in arterial walls and blood plasma in atherosclerotic rabbits (5). PCOOH was also identified in human atherosclerotic lesions (6, 7). Furthermore, PCOOH accumulation in plasma has been shown in human subjects with pathological conditions such as hyperlipidemia (8, 9), diabetes (10), uremia (9), and alcoholism (11). Because hyperlipidemia and diabetes are strongly associated with increased incidence of atherosclerosis (12-14), higher plasma PCOOH conditions in these patients may be involved in atherogenesis.In the course of phospholipid oxidation, PC is primarily oxidized to PCOOH. Further oxidative modification of PCOOH yields various secondary oxidation products. To date, a number of the secondary oxidation products have been reported to mediate several atherogenic processes (15, 16). For instance, a series of oxidized PCs with a truncated sn-2 acyl group (sn-2-truncated PCs), such as 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine, activate aortic endothelial cell binding to monocytes (17-19). The sn-2-truncated PCs with a terminal aldehyde gr...

show abstract

mentioning

confidence: 98%

Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1

Asai

Okajima

Nakagawa

et al. 2009

Journal of Lipid Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…Although hypercholesterolemic rabbits have been generally used for the study of atherosclerosis, there had been no report of AGE accumulation in their atherosclerotic aortas before our previous report 24) except for 2-(2-furoyl)-4(5)-(2-furanyl)-1H-imidazole whose presence in vivo is still controversial. 25) In the present study, we examined old well-known AGEs, i.e., CML and pyrraline, and a relatively new AGE structure, argpyrimidine in cholesterol and fructose-fed rabbits.…”

Section: Deposition Of Ages In Atherosclerotic Lesionsmentioning

confidence: 99%

“…Similar acceleration of oxidative stress has been observed previously in cholesterol-fed rabbits. 16,17,23,24) This enhanced oxidative stress has been reported to be explained by the increase of NADPH oxidase which forms superoxide anion in artery. 30) Oxidative stress not only accelerates formation of some AGEs including CML from Amadori products but also promotes formation of glyoxal and suppresses detoxification of a-ketoaldehydes by glyoxalase, 29) leading to the acceleration of carbonyl stress.…”

Section: Deposition Of Ages In Atherosclerotic Lesionsmentioning

confidence: 99%

“…26,27) Consequently, CML and pyrraline were found to accumulate in the atherosclerotic aortas of the control cholesterol and fructose-fed New Zealand White rabbits as in humans and cholesterol and fructose-fed Japanese White rabbits. 24) In addition, argpyrimidine remarkably accumulated with intimal thickening. No data has been reported to date on the accumulation of argpyrimidine in atherosclerotic aortas although the AGE structure has been found in intima and media of small artery wall of kidney from diabetic patients.…”

Section: Deposition Of Ages In Atherosclerotic Lesionsmentioning

confidence: 99%

“…25) In the present study, we examined old well-known AGEs, i.e., CML and pyrraline, and a relatively new AGE structure, argpyrimidine in cholesterol and fructose-fed rabbits. Fructose was given in addition to cholesterol in order to accelerate the formation of AGEs related to atherosclerotic lesions 24) because fructose promotes in vitro AGE formation about 8-10 times faster than glucose. 26,27) Consequently, CML and pyrraline were found to accumulate in the atherosclerotic aortas of the control cholesterol and fructose-fed New Zealand White rabbits as in humans and cholesterol and fructose-fed Japanese White rabbits.…”

Section: Deposition Of Ages In Atherosclerotic Lesionsmentioning

confidence: 99%

See 2 more Smart Citations

Inhibitory Effects of Amlodipine and Fluvastatin on the Deposition of Advanced Glycation End Products in Aortic Wall of Cholesterol and Fructose-Fed Rabbits

Akira

Amano

Okajima

et al. 2006

Biological & Pharmaceutical Bulletin

Self Cite

View full text Add to dashboard Cite

Recent studies suggest that advanced glycation end products (AGEs) can promote the development of atherosclerotic lesions in a similar manner to oxidatively modified low density lipoproteins. As oxidative stress accelerates the formation of AGEs, antioxidant drugs may exert atheroprotective effects via suppression of AGE formation. Although amlodipine, a calcium channel blocker, and fluvastatin, a 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, show antioxidant and atheroprotective effects, the relation of AGEs to their effects is unknown. We immunohistochemically investigated the inhibitory effects of chronic treatment with amlodipine (5 mg/kg per day) or fluvastatin at a dose insufficient to reduce plasma cholesterol levels (2 mg/kg per day) on the accumulation of AGEs in atherosclerotic aortas of rabbits fed 1% cholesterol diet and 10% fructose containing water. After eight weeks of treatment, AGEs, namely argpyrimidine, carboxymethyllysine and pyrraline, markedly accumulated with intimal thickening in cholesterol and fructose-fed control rabbits, while the drugs inhibited those changes other than the pyrraline deposition without plasma lipid-lowering effects. Enhanced lipid peroxidation was observed in plasma from cholesterol and fructose-fed rabbits only, and lipid peroxidation was not suppressed by the drugs. These results suggest that the atheroprotective effects of the drugs are at least partly due to the suppression of AGE accumulation although the exact mechanism of AGE suppression is ambiguous.

show abstract

The molecular mechanisms underpinning the therapeutic properties of oleanolic acid, its isomer and derivatives for type 2 diabetes and associated complications

Camer

Szabo

et al. 2014

Molecular Nutrition Food Res

View full text Add to dashboard Cite

X. (2014). The molecular mechanisms underpinning the therapeutic properties of oleanolic acid, its isomer and derivatives for type 2 diabetes and associated complications. Molecular Nutrition and Food Research, 58 (8), 1750-1759. The molecular mechanisms underpinning the therapeutic properties of oleanolic acid, its isomer and derivatives for type 2 diabetes and associated complications AbstractRecent research has uncovered the molecular mechanisms responsible for the therapeutic properties of oleanolic acid (OA), its isomer ursolic acid (UA), and derivatives. In particular, recent reports have highlighted the benefits of these compounds in the prevention and treatment of type 2 diabetes and associated life-threatening complications, such as nonalcoholic fatty liver disease, nephropathy, retinopathy, and atherosclerosis. The prevalence of type 2 diabetes is of major concern since it is reaching global epidemic levels. Treatments targeting the signaling pathways altered in type 2 diabetes are being actively investigated, and OA and UA in natural and derivative forms are potential candidates to modulate these pathways. We will explore the findings from in vitro and in vivo studies showing that these compounds: (i) improve insulin signaling and reduce hyperglycemia; (ii) reduce oxidative stress by upregulating anti-oxidants and; (iii) reduce inflammation by inhibiting proinflammatory signaling. We will discuss the molecular mechanisms underpinning these therapeutic properties in this review in order to provide a rationale for the future use of OA, UA, and their derivatives for the prevention and treatment of type 2 diabetes and associated comorbidities. Abstract: Recent research has uncovered the molecular mechanisms responsible for the therapeutic properties of oleanolic acid (OA), its isomer ursolic acid (UA) and derivatives. In particular, recent reports have highlighted the benefits of these compounds in the prevention and treatment of type 2 diabetes and associated life-threatening complications, such as nonalcoholic fatty liver disease, nephropathy, retinopathy and atherosclerosis. The prevalence of type 2 diabetes is of major concern since it is reaching global epidemic levels. Treatments targeting the signalling pathways altered in type 2 diabetes are being actively investigated, and OA and UA in natural and derivative forms are potential candidates to modulate these pathways. We will explore the findings from in vitro and in vivo studies showing that these compounds: 1) Improve insulin signalling and reduce hyperglycaemia; 2) Reduce oxidative stress by upregulating anti-oxidants and; 3) Reduce inflammation by inhibiting proinflammatory signalling. We will discuss the molecular mechanisms underpinning these therapeutic properties in this review in order to provide a rationale for the future use of OA, UA and their derivatives for the prevention and treatment of type 2 diabetes and associated comorbidities.

show abstract

Fructose Ingestion Enhances Atherosclerosis and Deposition of Advanced Glycated End-products in Cholesterol-fed Rabbits

Cited by 30 publications

References 32 publications

Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1

Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1

Inhibitory Effects of Amlodipine and Fluvastatin on the Deposition of Advanced Glycation End Products in Aortic Wall of Cholesterol and Fructose-Fed Rabbits

The molecular mechanisms underpinning the therapeutic properties of oleanolic acid, its isomer and derivatives for type 2 diabetes and associated complications

Contact Info

Product

Resources

About