scholarly journals Dietary polyunsaturated fat intake is associated with low-density lipoprotein size, but not with susceptibility to oxidation in subjects with impaired glucose metabolism and type II diabetes: the Hoorn study

2006 ◽  
Vol 61 (2) ◽  
pp. 205-211 ◽  
Author(s):  
G Bos ◽  
M C Poortvliet ◽  
P G Scheffer ◽  
J M Dekker ◽  
M C Ocke ◽  
...  
2005 ◽  
Vol 109 (2) ◽  
pp. 189-197 ◽  
Author(s):  
Mike J. Sampson ◽  
Simon Braschi ◽  
Gavin Willis ◽  
Sian B. Astley

The HDL (high-density lipoprotein)-associated enzyme PON (paraoxonase)-1 protects LDL (low-density lipoprotein) from oxidative modification in vitro, although it is unknown if this anti-atherogenic action occurs in vivo. In a cross-sectional study of 58 Type II diabetic subjects and 50 controls, we examined the fasting plasma LDL basal conjugated diene concentration [a direct measurement of circulating oxLDL (oxidatively modified LDL)], lipoprotein particle size by NMR spectroscopy, PON-1 polymorphisms (coding region polymorphisms Q192R and L55M, and gene promoter polymorphisms −108C/T and −162G/A), PON activity (with paraoxon or phenyl acetate as the substrates) and dietary antioxidant intake. Plasma oxLDL concentrations were higher in Type II diabetic patients (males, P=0.048; females, P=0.009) and unrelated to NMR lipoprotein size, PON-1 polymorphisms or PON activity (with paraoxon as the substrate) in any group. In men with Type II diabetes, however, there was a direct relationship between oxLDL concentrations and PON activity (with phenyl acetate as the substrate; r=0.611, P=0.0001) and an atherogenic NMR lipid profile in those who were PON-1 55LL homozygotes. Circulating oxLDL concentrations in vivo were unrelated to PON-1 genotypes or activity, except in male Type II diabetics where there was a direct association between PON activity (with phenyl acetate as the substrate) and oxLDL levels. These in vivo data contrast with in vitro data, and may be due to confounding by dietary fat intake. Male Type II diabetic subjects with PON-1 55LL homozygosity have an atherogenic NMR lipid profile independent of LDL oxidation. These data do not support an in vivo action of PON on LDL oxidation.


1981 ◽  
Vol 241 (1) ◽  
pp. E57-E63 ◽  
Author(s):  
J. D. Turner ◽  
N. A. Le ◽  
W. V. Brown

The mechanism of change in low-density lipoprotein (LDL) levels by diets differing in fat saturation have been studied. Turnover of 125I-LDL was measured in eight subjects with type II hyperlipoproteinemia and in seven normal control subjects during two dietary periods containing 40% of calories as either safflower oil (polyunsaturated fat, PSF) or as lard (saturated fat, SF). Higher levels of LDL apoprotein and LDL-cholesterol were observed in both groups on saturated fat. Subjects with elevated LDL levels (type II) showed a more marked effect of polyunsaturated fat with 25% lower LDL production rate as compared to a reduction of only 10% for the control group. On the PSF diet, the production rate in type II (12.7 mg.kg-1.day-1) was not statistically different from normal subjects (10.5 mg.kg-1.day-1). On this diet, the higher levels of LDL cholesterol in the type II subjects (as compared to controls) were due to a lower fractional clearance rate, mean of 0.27/day compared to a mean of 0.39/day for the normal subjects. Although individuals with type II hyperlipoproteinemia may have a primary clearance defect, the major reduction in plasma cholesterol concentrations achieved with a diet high in polyunsaturated fat can be attributed to a significantly lower LDL production.


2003 ◽  
Vol 105 (5) ◽  
pp. 591-599 ◽  
Author(s):  
Dragos VINEREANU ◽  
Eleftherios NICOLAIDES ◽  
Ann C. TWEDDEL ◽  
Christoph K. MÄDLER ◽  
Ben HOLST ◽  
...  

The aim of the present study was to measure regional ventricular function at rest and during stress in order to assess if patients with Type II diabetes have subclinical myocardial dysfunction and if it is related to risk factors. Seventy subjects (35 patients with Type II diabetes with no symptoms, signs or history of heart disease, and 35 age- and sex-matched healthy controls) had echocardiography at rest and during dobutamine stress. Myocardial velocities were measured off-line from digital loops of colour tissue Doppler. Subendocardial function was assessed from the mean longitudinal velocities of four basal segments (apical views) and radial function from the velocities of the basal posterior wall (parasternal view). Systolic functional reserve was calculated as the increase in velocity from baseline. Longitudinal peak systolic velocity was lower in patients with diabetes, at rest (5.6±1.4 compared with 6.5±1.1 cm/s) and at peak stress (10.9±2.8 compared with 14.3±2.1 cm/s) (both P<0.01). Functional reserve was impaired in patients with diabetes (+5.4±2.0 compared with +7.7±1.7 cm/s; P<0.01). Radial systolic velocity was higher in patients with diabetes (5.4±1.3 compared with 4.7±1.4 cm/s; P<0.05). Resting longitudinal systolic function correlated inversely with low-density lipoprotein—cholesterol (r=-0.53), glycated haemoglobin (r=-0.48), age (r=-0.41) and diastolic blood pressure (r=-0.38) (all P<0.05). Peak stress systolic velocity correlated inversely with glycated haemoglobin (r=-0.46) and age (r=-0.44) (both P<0.01). In conclusion, patients with Type II diabetes and no clinical heart disease have impaired subendocardial function of the left ventricle at rest and peak stress, which is related to glycated haemoglobin and serum low-density lipoprotein—cholesterol.


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