Enhanced susceptibility of low-density lipoprotein to in vitro oxidation in type 1 and type 2 diabetic patients

Beaudeux, Jean-Louis; Guillausseau, Pierre-Jean; Peynet, Jacqueline; Flourie, F.; Assayag, Michel; D, Tielmans; Warnet, A; Rousselet, F

doi:10.1016/0009-8981(95)06106-n

Cited by 38 publications

(26 citation statements)

References 37 publications

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“…Enhanced oxidative stress, as monitored by increased levels of plasma hydroperoxides [20][21][22][23][24] and increased susceptibility of LDL to oxidation, has already been reported in diabetic patients [24,29]. In diabetic patients in poor control, excess glucose causes an enhancement of the glycation of plasma protein and this non-enzymatic glycation of proteins has been presumed to cause enhanced oxidative stress, through generation of oxygen free radicals [16][17][18][19].…”

Section: Discussionmentioning

confidence: 99%

“…This non-enzymatic glycation of proteins has been presumed to cause an enhanced oxidative stress, through generation of oxygen free radicals [16][17][18][19]. An enhanced oxidative stress, i. e. increased levels of plasma hydroperoxides, has actually been observed in NIDDM [20][21][22][23][24]. The augmented generation of free radicals could also result in oxidative damage of LDL, the known potentially atherogenic properties of oxidized LDL including monocyte recruitment [25] and modulation of expression of adhesion molecules [26,27].…”

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confidence: 99%

“…The augmented generation of free radicals could also result in oxidative damage of LDL, the known potentially atherogenic properties of oxidized LDL including monocyte recruitment [25] and modulation of expression of adhesion molecules [26,27]. Enhanced susceptibility of LDL to oxidation has recently been reported in diabetic patients [24,28,29].…”

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confidence: 99%

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E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

Cominacini¹,

Pasini²,

Garbin³

et al. 1997

Diabetologia

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Atherosclerosis is the major cause of death in patients with diabetes mellitus, accounting for more than 70 % of mortality in all forms of the disease [1,2]. There is plenty of evidence that monocytes are involved in the pathogenesis of atherosclerosis [3,4], the earliest morphological evidence of the disease being the binding of monocytes to the endothelium [5][6][7]. This adhesion of monocytes, a prerequisite for their recruitment and accumulation in the lesion, is probably due to the appearance of adhesion Diabetologia (1997) Summary Although elevated levels of soluble E-selectin and intercellular cell adhesion molecules-1 (ICAM-1) have been reported in non-insulin-dependent diabetes mellitus (NIDDM), it is not clear by what mechanism this elevation occurs and whether or not it is related to glycaemic control. In this study we analyse: 1) the relation of glycaemic control with the concentrations of E-selectin, vascular cell adhesion molecules-1 (VCAM-1) and ICAM-1 in NIDDM patients; 2) whether metabolic control can affect the oxidative stress (as measured by plasma hydroperoxide concentration and susceptibility of LDL to in vitro oxidation) and hence the adhesion molecule plasma concentrations. Thirty-four (19 males and 15 females) poorly controlled NIDDM patients were studied. All parameters were evaluated at the beginning of the study and after 90 days of dietary and pharmacological treatment. The treatment decreased HbA 1C (p < 0.001), E-selectin (p < 0.001), plasma hydroperoxides (p < 0.003) and the susceptibility of LDL to in vitro oxidation (lag phase) (p < 0.0001). Before treatment HbA 1C , lag phase and lipid hydroperoxides correlated with E-selectin plasma concentration (r = 0.51, -0.57 and 0.54, respectively, p < 0.01). There was also a correlation between HbA 1C and lag phase (p < 0.01) and between HbA 1C and lipid hydroperoxides (p < 0.01). In addition, the variations of HbA 1C , lag phase and lipid hydroperoxide values correlated with those for E-selectin concentration after 90 days' treatment (r = 0.54, -0.64 and 0.61, respectively, p < 0.01). In multiple linear correlation analysis, however, the partial correlation coefficients of HbA 1C (basal and variations) with Eselectin concentration (basal and variations) fell to non-significant values (r = 0.12 and 0.25, respectively) when LDL lag phase and plasma hydroperoxides were kept constant. The results indicate that the improvement of metabolic control in NIDDM patients is associated with a decrease of E-selectin plasma levels; they also suggest that glycaemic control per se is not directly implicated in determining E-selectin plasma concentration; glycaemic control could affect E-selectin concentration through its effect on oxidative stress. [Diabetologia (1997) 40: 584-589]

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

Cominacini¹,

Pasini²,

Garbin³

et al. 1997

Diabetologia

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“…In most cases, LDL from NIDDM patients is more susceptible to oxidation [12-14, 19, 46], probably reflecting the well-known diminished resistance to oxidation of small LDL particles [26] which is increased in these patients [25]. Regarding IDDM subjects, most studies [15][16][17][18] were performed in patients with diabetes of long duration (10 years or more) and displayed increased LDL susceptibility to oxidation when compared to control subjects. Those studies describing decreased [20] or no difference [21,47] in LDL susceptibility to oxidation between IDDM and control subjects, did not report the duration of the disease.…”

Section: Discussionmentioning

confidence: 99%

“…Several groups have reported increased susceptibility to oxidation of LDL isolated from diabetic patients [12][13][14][15][16][17][18][19], although other authors disagree [20,21]. In particular, studies carried out in IDDM subjects that showed higher susceptibility to oxidation [15][16][17][18] have been performed in patients with diabetes of more than 10 years duration.…”

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Electronegative low density lipoprotein subform is increased in patients with short-duration IDDM and is closely related to glycaemic control

et al. 1996

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Atherosclerosis is the major cause of death in the diabetic population. Hyperglycaemia per se is an independent risk factor for the development of cardiovascular disease, in spite of the coexistence of other known risk factors, such as hyperlipidaemia and hypertension [1,2]. Elevated concentrations of low density lipoproteins (LDL) are also a major risk factor in the general population [3,4]. However, LDL levels are usually normal in both insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes (NIDDM) [2,5].It has been postulated that the increased cardiovascular risk for diabetic patients could be related, among other factors, to LDL qualitative modifications such as oxidation and glycation. These modifications impair LDL cellular catabolism, leading to loss of affinity for LDL receptors in fibroblasts, increased accumulation of cholesteryl esters in macrophages, and immunological responses [6,7]. In Diabetologia (1996) Summary We evaluated the effect of improving glycaemic control with intensive insulin therapy on LDL susceptibility to oxidation, electronegative LDL proportion, and LDL subfraction phenotype in a group of 25 patients with short-duration insulin-dependent diabetes mellitus (IDDM); 25 matched healthy control subjects were also studied. LDL susceptibility to oxidation was measured by continuous monitoring of conjugated diene formation. Electronegative LDL was isolated by anion exchange chromatography, and quantified as percentage of total LDL. Six LDL subfractions were isolated by density gradient ultracentrifugation and phenotype A or B classified as the quotient (LDL1-LDL3)/(LDL4-LDL6). Compared to the control group, IDDM subjects with poor glycaemic control showed higher electronegative LDL (19.03 ± 10.09 vs 9.59 ± 2.98 %, p < 0.001), similar LDL subfraction phenotype and lower susceptibility to oxidation (lag phase 45.6 ± 8.8 vs 41.2 ± 4.7 min, p < 0.05). After three months of intensive insulin therapy, HbA 1 c decreased from 10.88 ± 2.43 to 5.69 ± 1.54 % (p < 0.001), and electronegative LDL to 13.84 ± 5.15 % (p < 0.05). No changes in LDL susceptibility to oxidation or LDL subfraction phenotype were observed. Electronegative LDL appeared significantly correlated to HbA 1 c and fructosamine (p < 0.01 and p < 0.001) only in poorly controlled IDDM patients. These findings suggest that high electronegative LDL in IDDM subjects is related to the degree of glycaemic control, and could therefore be due to LDL glycation rather than to LDL oxidation or changes in LDL subfraction phenotype.

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Reverse cholesterol transport in diabetes mellitus

Quintão

Medina

Passarelli

2000

Diabetes Metab. Res. Rev.

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There are epidemiological data and experimental animal models relating the development of premature atherosclerosis with defects of the reverse cholesterol transport (RCT) system. In this regard, the plasma concentrations of the high density lipoprotein (HDL) subfractions, of cholesteryl ester transfer protein (CETP), as well as the activity of the enzyme lecithin-cholesterol acyl transferase (LCAT) play critical roles. However, there has been plenty of evidence that atherosclerosis in diabetes mellitus (DM) is ascribed to a greater arterial wall cell uptake of modified apoB-containing lipoproteins whereas a primary or predominant defect of the RCT system is still a subject of debate. In other words, in spite of the fact that in DM the composition and rates of metabolism of the HDL particles are greatly altered and display a diminished in vitro efficiency to remove cell cholesterol, definitive in vivo demonstration of the importance of this fact in atherogenesis is lacking. Furthermore, the roles played by LCAT and CETP in RCT in DM are difficult to interpret because the in vitro procedures of measurement utilized have either been inadequate, or inappropriately interpreted. Knock-out or transgenic mice are much needed models to investigate the roles of LCAT, CETP, phospholipid transfer protein (PLTP), and of a CETP inhibitor in the development of atherosclerosis of experimental DM.

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Enhanced susceptibility of low-density lipoprotein to in vitro oxidation in type 1 and type 2 diabetic patients

Cited by 38 publications

References 37 publications

E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

Electronegative low density lipoprotein subform is increased in patients with short-duration IDDM and is closely related to glycaemic control

Reverse cholesterol transport in diabetes mellitus

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