Modification of Lipoproteins in Diabetes

Lopes‐Virella, Maria F.; Klein, Richard L.; Virella, Gabriel

doi:10.1002/(sici)1099-0895(199603)12:1<69::aid-dmr158>3.0.co;2-b

Cited by 28 publications

(2 citation statements)

References 171 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These data suggest that LDL may be more modified in HD. In general, M-LDL is produced when protein glycation and glucose autoxidation generate free radicals and catalyze lipid per oxidation and means dense LDL, electronegatively charged LDL and Ox-LDL (32). During HD, these phenomena may occur.…”

Section: Discussionmentioning

confidence: 99%

Effects of Lipid Abnormalities on Arteriosclerosis and Hemostatic Markers in Patients under Hemodialysis

Kushiya

Wada

Sakakura

et al. 2003

Clin Appl Thromb Hemost

View full text Add to dashboard Cite

Vascular events caused by arteriosclerosis are the major cause of death in patients under hemodialysis (HD). Arteriosclerosis is associated with lipoprotein abnormalities such as increased serum levels of low-density lipoprotein (LDL), especially of modified LDL (M-LDL) and oxidized LDL (Ox-LDL). We examined the relationship between markers of arteriosclerosis, hemostasis, and lipid metabolism in patients with chronic renal failure, hyperlipidemia, and healthy volunteers. In patients under HD, the serum levels of total cholesterol, LDL, and triglyceride (TG) were decreased, but the serum levels of M-LDL were increased compared to HL and healthy volunteers. In patients with CRF, the serum levels of Ox-LDL in patients under HD were lower than in those under continuous ambulatory peritoneal dialysis or conservative therapy. The plasma levels of antithrombin and protein C were significantly lower and the plasma levels of thrombomodulin were significantly higher in patients under HD compared to those under conservative therapy. These data show that patients under HD were more in hypercoagulable state than those under conservative therapy. Among patients under HD, only the plasma levels of von Willebrand factor were significantly increased in patients with more than 30 U/L of Ox-LDL compared to those with less than 30 U/L of Ox-LDL. There was no significant difference in the tests of arteriosclerosis among M-LDL values and Ox-LDL values. These findings suggest that abnormalities of lipid are not the main risk factor for arteriosclerosis disease in patients under HD.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of Lipid Abnormalities on Arteriosclerosis and Hemostatic Markers in Patients under Hemodialysis

Kushiya

Wada

Sakakura

et al. 2003

Clin Appl Thromb Hemost

View full text Add to dashboard Cite

show abstract

“…The effects of biologic agents such as cytokines and other hormones besides progesterone on macrophage lipoprotein and cholesterol metabolism have been examined in many model macrophage systems and are listed in Table 4. Interestingly, bacterial products such as lipopolysaccharide increase LDL uptake and macrophage cholesterol accumulation (263)(264)(265). However, in these studies it is not clear whether LDL uptake occurs secondary to macrophage recognition and uptake of bacterial products that have formed complexes with LDL, or whether the bacterial product stimulates direct LDL uptake (266).…”

Section: Modulation Of Foam Cell Cholesterol Metabolismmentioning

confidence: 99%

Macrophage foam cells and atherosclerosis

Kruth

2001

Front Biosci

View full text Add to dashboard Cite

Focal buildup of cholesterol in arteries is the process that produces atherosclerotic plaques, the cause of most coronary artery disease and strokes. Monocyte-derived macrophages are central cells that accumulate this cholesterol in atherosclerotic lesions, a manifestation of the scavenging function of the macrophage. Different types of cholesterol-containing lipid particles found in atherosclerotic lesions may enter macrophages by a variety of endocytic pathways. The fate of cholesterol that enters macrophages determines whether macrophages help or hinder cholesterol removal from the vessel wall. Macrophages may function to carry cholesterol out of lesions, or to process the cholesterol for excretion in association with small protein-phospholipid complexes. Alternatively, macrophages that do not efficiently function to remove cholesterol from lesions may ultimately undergo cell death. Some cytokines, hormones, and pharmacologic agents show potential to modulate these processes and may be useful in directing macrophage function in atherosclerotic lesions towards beneficial rather than harmful effects.

show abstract