Adipokine serum concentrations, anthropometric measurements and socio-economic status in two ethnic groups with different prevalence levels for cardiovascular diseases and type 2 diabetes.

Obesity is more common in African than Asian-Indian populations and yet type 2 diabetes and cardiovascular diseases are more common in the latter populations. The main purpose of the current study was therefore to determine whether ethnic differences in body fat distribution, adipokine levels, and socio-economic status may explain population differences in the prevalence of these metabolic disorders. Leptin, IL-6, CRP, visceral fat, education level, and socio-economic status were measured in 50 African and the same number of Indian women residing in Johannesburg, South Africa. Serum leptin levels were significantly higher in Indian than African subjects (41.3±2.0 and 34.2±2.9 ng/ml, respectively; p<0.05). TNF-α levels were significantly higher in the African group, (5.22±0.86 vs. 2.54±0.52 pg/ml; p<0.05), whilst visceral fat levels were significantly lower (56.1±5.5 vs. 77.9±6.5 cm(2); p<0.05). The CRP and IL-6 levels were not different between groups. Education levels (p<0.005) and socio-economic status (p<0.0001) were both lower in the African subjects, however, adjusting for these variables in ANCOVA did not attenuate differences in adipokine or visceral fat levels. We hypothesise that one of the reasons for the higher prevalence of obesity in the African than Indian population may be related to lower leptin levels, whilst ethnic differences in the prevalence of metabolic disorders cannot be explained by differences in adipokine levels, but maybe related to higher visceral adiposity in the Indian group.

Quantity versus quality of LDL cholesterol in patients with familial hypercholesterolemia--which is more important?

BACKGROUND: The aim of this study was to determine the effects of low-density lipoprotein (LDL) particle size and composition on the susceptibility of LDL to oxidation in subjects with Familial Hypercholesterolemia (FH). METHODS: LDL was isolated from 20 FH homozygotes, 20 FH heterozygotes and 20 normal controls. Susceptibility of LDL to ex vivo copper-mediated oxidation was assessed by measuring conjugated diene production at 234 nm. Other factors known to influence LDL oxidation, namely particle size, vitamin E levels, and fatty acid composition of the LDL particles were also measured. RESULTS: The mean duration of the lag phase was 1.42-fold longer in the FH homozygotes, and 1.21-fold longer in the FH heterozygotes than in the normal controls. LDL particle size was significantly larger in the FH homozygotes (26.45+/-0.37 nm) and FH heterozygotes (26.01+/-0.40 nm) compared to the normal control group (25.17+/-0.39 nm). LDL vitamin E concentrations, when expressed relative to LDL cholesterol concentrations, were similar in all the groups. In addition, no significant differences were observed in the total saturated, monounsaturated or polyunsaturated fatty acid content of LDL in the three groups of subjects. CONCLUSION: These results suggest that it is the great excess in LDL quantity, rather than LDL 'quality', that is responsible for the severe and premature atherosclerosis in patients with FH.

Cell adhesion molecules - can they be used to predict coronary artery disease in patients with familial hypercholesterolaemia?

Adhesion of leukocytes to endothelial cells via cell adhesion molecules (CAMS) is thought to be pivotal in the initiation of atherosclerosis. As patients with familial hypercholesterolaemia (FH) are known to develop severe, premature coronary artery disease (CAD), we investigated the usefulness of soluble forms of CAMS namely vascular cellular adhesion molecule-1 (VCAM), intercellular cell adhesion molecule-1 (ICAM) and E-selectin as predictive markers of the presence and severity of atherosclerosis in this patient group. Twenty heterozygous FH patients without CAD; 24 heterozygous FH patients with CAD; 17 homozygous FH patients without documented CAD; nine homozygous FH patients with overt CAD; and 50 healthy controls were studied. Carotid artery intima media thickness (IMT) was also measured in the homozygous patients. Levels of the adhesion molecules VCAM, ICAM and E-selectin were not significantly elevated in homozygous FH patients and heterozygous FH patients, both with and without CAD, compared to the normal control subjects. In addition the range of results was so wide and the overlap of values with normal controls so great, that the use of an individual level of either VCAM, ICAM or E-selectin was not predictive of either the presence or degree of atherosclerosis in the FH subjects.

Auto-antibodies against oxidized LDL as a marker of coronary artery disease in patients with familial hypercholesterolaemia.

Auto-antibodies to oxidized low-density lipoprotein (ox-LDL) are thought to play a pivotal role in the pathogenesis of atherosclerosis. This study investigates the value of auto-antibodies to ox-LDL as a predictive marker of atherosclerosis in patients with both homozygous and heterozygous familial hypercholesterolaemia (FH), who are known to suffer from severe premature atherosclerosis. The influences of well-established risk factors for atherosclerosis such as age, LDL-cholesterol levels and smoking on the results were also determined. Auto-antibody titres to ox-LDL and fasting lipid profiles were measured in 26 homozygous FH patients, 20 heterozygous FH patients without documented coronary artery disease (CAD), 24 heterozygotes with overt CAD and 10 healthy normocholesterolaemic controls. Carotid intima media thickness, used as an in vivo assessment of atherosclerosis, was also measured in the homozygous FH patients. Ox-LDL titres did not differ between the groups. There was also no association between ox-LDL titres and the LDL-cholesterol level (P=0.14), presence or absence of CAD (P=0.69), age (P=0.50), carotid intima-media thickness (P=0.51) or smoking (P=1.0). In conclusion, antibody titres against ox-LDL cannot be used as a predictive marker of the presence or severity of atherosclerosis in patients with FH.