<b>Structural and compositional modifications of diabetic low‐density lipoproteins influence their receptor‐mediated uptake by hepatocytes</b>

Krämer-Guth, Annette; Quaschning, Thomas; Galle, Jan; Baumstark, Manfred W.; Königer, M.; Nauck, Matthias; Schollmeyer, P.; März, Winfried; Wanner, C

doi:10.1046/j.1365-2362.1997.1460695.x

Cited by 30 publications

(30 citation statements)

References 31 publications

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“…These lipoprotein modifications can contribute to the increased risk of coronary atherosclerosis (CHD) associated with diabetes [1,2]. These observations led us to agree with other authors [24] who supposed that glyc-LDL could be used as a sensitive index of short-to-long term glycemic control in diabetes [32,33].…”

Section: Discussionsupporting

confidence: 83%

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In vivo oxidizability of LDL in type 2 diabetic patients in good and poor glycemic control

et al. 2004

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We aimed to determine if increased non-enzymatic glycosylation of the LDL was sufficient to increase the susceptibility to in vivo oxidation of the LDL particles. Twenty-two type 2 diabetic patients (11 males and 11 females) were included in this study. They were enrolled on the basis of good [glycated hemoglobin (HbA 1c ) < 7%] and poor glycemic control [(HbA 1c ) > 8%]. LDL were isolated by sequential ultracentrifugation and analyzed by capillary electrophoresis (CE) for diene conjugate content and for electronegativity. The glyc-LDL levels were increased in all diabetic type 2 patients, peaking in the diabetic subjects in poor diabetic control (17.3 ± 8.07%). The LDL content of diene conjugates was similar between the two groups (6.65 ± 0.77% for the patients with good glycemic control versus 6.88 ± 0.74% for those with poor glycemic control; P = 0.49) as was the electrophoretic mobility ((−1.14544 ± 0.089) × 10 −4 cm 2 /(V s) for the patients with good glycemic control and (−1.13666 ± 0.073) × 10 −4 cm 2 /(V s) for those with poor glycemic control; P = 0.80).The susceptibility to in vivo oxidation of LDL from type 2 diabetic patients in poor glycemic control did not differ from that of well-controlled diabetic patients. LDL glycosylation was not able to increase the oxidizability of LDL in the diabetic patients with poor glycemic control.

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Section: Discussionsupporting

confidence: 83%

“…The increased atherogenic risk associated with diabetes is accentuated by the numerous differences described between lipoproteins from diabetic and non-diabetic individuals [1,2]. Because of hyperglycemia most plasma apolipoproteins from diabetic subjects become glycosylated and impaired in their biological function [3].…”

Section: Introductionmentioning

confidence: 99%

In vivo oxidizability of LDL in type 2 diabetic patients in good and poor glycemic control

et al. 2004

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“…A delayed chylomicron and VLDL clearance has been identified in patients with type 2 diabetes and in adult patients with DM1 (11,12) and this could play a role in hypertriglyceridemia. Increased production of LDL from elevated VLDL and delayed clearance of (glycosylated) LDL could lead to hypercholester- (35,36). A reduced hepatic uptake of LDL particles from patients with type 2 diabetes was associated with an altered lipid composition of the LDL particle and glycosylation of LDL protein (36).…”

Section: Discussionmentioning

confidence: 99%

Postprandial Chylomicron Clearance Rate in Late Teenagers with Diabetes Mellitus Type 1

Waarde¹,

Odink²,

Rouwé³

et al. 2001

Pediatr Res

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A delayed chylomicron (CM) clearance rate, a known risk factor for atherosclerosis, has been described in adults with diabetes type 1 (DM1). We determined the CM clearance rate in late teenagers with DM1, and the relationship between CM clearance rate and elevated plasma lipid concentrations in DM1 teenagers in poor metabolic control (as characterized by HbA 1c percentage). Plasma lipids and CM clearance were determined in nine patients with DM1 (mean age Ϯ SD: 17.5 Ϯ 0.6 y) and four healthy controls (mean age Ϯ SD: 20.1 Ϯ 0.8 y), by measuring breath 13 CO 2 , plasma triglyceride, retinyl palmitate, and 13 Clabeled oleic acid concentrations, after oral administration of a fat-rich meal together with vitamin A and 13 C-oleic acid. In patients with DM1, fasting triglyceride and cholesterol concentrations were positively correlated with HbA 1c percentage (p Ͻ 0.05). Neither in DM1 patients, nor in controls, was an elevated triglyceride concentration (above 1.7 mmol/L) found. Yet, in 22% of DM1 patients, cholesterol concentration was above 5.2 mmol/L, but not in any of the controls. CM clearance rate in DM1 patients was similar to that in controls and did not signif- Diabetes mellitus type 1 (DM1) is associated with a 2-4 fold increased risk for cardiovascular disease (1). Specific diabetesrelated phenomena have been suggested to play a role in the observed association, such as glycosylation of proteins (2), presence of renal disease (3), elevated concentrations of plasma cholesterol, triglycerides, and low density lipoprotein (LDL) cholesterol (4), and altered composition of very low density lipoprotein (VLDL) and LDL (5, 6). In children and late teenagers, studies on risk factors associated with DM1 and atherosclerosis have mainly focused on cholesterol and triglyceride concentrations (7-9). Elevated concentrations of both cholesterol and triglycerides have been reported in children with DM1 in poor metabolic control, which tended to decrease to nondiabetic values upon improvement of metabolic control (7-9).A delayed chylomicron (CM) clearance has been identified as a risk factor for atherosclerosis in patients with coronary heart disease, in patients with type 2 diabetes, and in adult patients with DM1 (10 -12). Insulin enhances the metabolism of CM by stimulating the hydrolysis of CM triglycerides by lipoprotein lipase and the hepatic uptake of CM remnants (11). A relative deficiency of insulin, such as present in DM1, could therefore lead to a delay in CM clearance. A delay in CM clearance would imply a prolonged postprandial hyperlipidemia, which supposedly leads to increased deposition of CM contents into the arterial wall and to an unfavorable translocation of cholesteryl-esters from HDL to CM (13,14). Delays in CM clearance are amenable to dietary intervention, by changing the intake of fish oil (long chain PUFA) (15), monounsaturated-fat (16)

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“…In moderately severe Type II diabetes, the decrease of LDL catabolism is multifactorial. The glycation of apoB [29,30], as well as the small size and the triglyceride enrichment of LDL in Type II diabetic subjects [30±33] have been shown to diminish the affinity of these particles to their receptor. The improvement of glycaemic control as assessed by the decrease of both HbA 1c and fasting glycaemia in our patients is consistent with a lesser apoB glycation and subsequently a greater affinity of LDL to their receptor.…”

Section: Discussionmentioning

confidence: 99%

Significant improvement of apolipoprotein B-containing lipoprotein metabolism by insulin treatment in patients with non-insulin-dependent diabetes mellitus

et al. 2000

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Cardiovascular diseases are the most common complications observed in Type II (non-insulin-dependent) diabetes mellitus [1]. The multiple abnormalities in lipoprotein metabolism frequently associated with Type II diabetes play an important part in the premature development of atherosclerosis in Type II diabetic patients. They generally have an increased plasma concentration of very low density lipoprotein (VLDL) particles that has been linked both to an increased synthetic rate and a decreased catabolic rate Diabetologia (2000)

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Structural and compositional modifications of diabetic low‐density lipoproteins influence their receptor‐mediated uptake by hepatocytes

Cited by 30 publications

References 31 publications

In vivo oxidizability of LDL in type 2 diabetic patients in good and poor glycemic control

In vivo oxidizability of LDL in type 2 diabetic patients in good and poor glycemic control

Postprandial Chylomicron Clearance Rate in Late Teenagers with Diabetes Mellitus Type 1

Significant improvement of apolipoprotein B-containing lipoprotein metabolism by insulin treatment in patients with non-insulin-dependent diabetes mellitus

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