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OBJECTIVE: To investigate whether improvements in cardiovascular risk factors, as observed in energy-balance conditions after exchanging carbohydrates (CHO) for monounsaturated (MUFA) fats, are also observed in energy-restricted conditions. DESIGN: Longitudinal, clinical intervention study using two types of energy-restricted diets (-30% of initial energy intake) with similar levels of saturated and polyunsaturated fats: a high CHO diet (55% of energy from CHOs, 10% from MUFAs) and a high MUFA diet (40% of energy from CHOs, 25% from MUFAs). SUBJECTS: A total of 32 overweight subjects (nine males, 23 females, BMI: 26-45 kg/m[SUP2]). MEASUREMENTS: Body weight, serum lipids, fasting plasma insulin and phospholipid fatty acid composition of red blood cells were measured at baseline and after 8 weeks. Various oxidative status parameters (plasma lipid hydroperoxides, total plasma antioxidant capacity, plasma uric acid and vitamin E) and serum-induced smooth muscular cell (SMC) proliferation were also measured at these time points. RESULTS: Weight loss (1.1 kg/week over the first 4 weeks and 6.7 kg at week 8) was not significantly affected by the diet composition. Both diets reduced significantly total serum cholesterol, but the MUFA-rich diet showed better effects on fasting serum triacylglycerol (TG) than the CHO-rich diet: 1.18 vs 1.51 mmol/l for the MUFA-rich diet (after vs before, P<0.05) and 1.42 vs 1.62 for the CHO-rich diet. After 8 weeks, plasma vitamin E concentrations were positively associated with the oleic acid level of red blood cell phospholipids and showed opposite variations in both diets (increase with the MUFA-rich diet and decrease with the CHO-rich diet). Relative changes in SMC proliferation induced by sera were negatively associated with the ratio oleic:linoleic acid of red blood cell phospholipids and were significantly higher with the CHO-rich diet. CONCLUSIONS: The MUFA-rich diet showed better effects on serum TG than the CHO-rich diet,... [ABSTRACT FROM AUTHOR]

OBJECTIVE: To study the associations of obesity (as body mass index (BMI)), of body fat distribution (as waist to hip ratio (WHR)) and of β-endorphinaemia (β-EP-aemia) with fasting insulin and glucose concentrations, with insulin secretion (as first phase insulin response (FPIR)) and with insulin sensitivity (S[sub I]) in obese women. DESIGN: a cross-sectional study of insulin sensitivity in obese women. SUBJECTS: 45 obese women (age: 20-70y, BMI: 27-50). MEASUREMENTS: Frequently sampled intravenous glucose tolerance test (FSIGTT), FPIR, fasting glucose, fasting insulin, BMI, body fat topography (WHR), β-EP-aemia, plasma ACTH. RESULTS: In univariate analysis the following positive associations were observed: fasting glucose with age and WHR, fasting insulin with BMI and WHR, β-EP plasma concentration with WHR; S[sub I] was negatively associated with BMI, WHR and β-EP plasma concentrations. This pattern of associations remained unaltered in multivariate analysis including age, BMI and WHR as independent variables. The contribution of β-EP plasma concentrations to Si variability was corroborated by a stepwise multiple regression analysis: 53.8% of S[sub I] variation could be explained by BMI (30.7%), by β-EP plasma concentrations (17.2%) and by WHR (5.9%). Finally, women were divided into two groups according to whether they had a peripheral (P-BFD, WHR ≤ 0.80, n=24) or an abdominal (A-BFD, WHR ≥ 0.85, n= 16) body fat distribution. After adjustment for age and BMI, S[sub l] values were lower while β-EP and ACTH plasma concentrations were higher in the A-BFD compared to the P-BFD group. In this latter group, 54.8% of S[sub l] variation was explained by the same variables as in the whole group. In the A-BFD group, higher WHR was associated with lower FPIR. CONCLUSIONS: 1) The major finding of this study is that, in non-diabetic obese women (especially those with a PBFD), higher β-EP plasma concentrations are... [ABSTRACT FROM AUTHOR]

Many mutations in the low density lipoprotein receptor gene (LDLR) have been characterized at the molecular level in individuals with familial hypercholesterolemia. Most of the mutations that have been reported are large deletions or insertions in the gene, it being much more difficult to identify point mutations. In this study, 139 unrelated French familial hypercholesterolemia subjects were screened for the presence of three different previously described LDLR point mutations, employing the polymerase chain reaction and allele-specific oligonucleotide hybridization. Only one subject carried a point mutation at amino acid position 792, which substituted a Trp codon for a Stop codon. The same mutation has previously been described in a subject originating from Saudi Arabia. Haplotype analysis of LDLR associated with each mutation was performed. The haplotypes were totally different, suggesting that this mutation has occurred more than once. [ABSTRACT FROM AUTHOR]