Argan Oil Exerts an Antiatherogenic Effect by Improving Lipids and Susceptibility of LDL to Oxidation in Type 2 Diabetes Patients.

In this study, we investigate the effect of argan oil consumption on serum lipids, apolipoproteins (AI and B), CRP, and LDL susceptibility to oxidation in type 2 diabetic patients which are known to have a high level of cardiovascular risk due to lipid abnormalities and lipid peroxidation. For that, 86 type 2 diabetic patients with dyslipidemia were randomized to one group consuming 25 mL/day of argan oil during 3 weeks and control group consuming 20 g/day of butter in breakfast. After argan oil intervention, serum triglycerides decreased by 11.84%, (P = 0.001), total chol by 9.13%, (P = 0.01), and LDL-chol by 11.81%, (P = 0.02). However, HDL-chol and Apo AI increased (10.51%, P = 0.01 and 9.40%, P = 0.045, resp.). Susceptibility of LDL to lipid peroxidation was significantly reduced by increasing of 20.95%, (P = 0.038) in lag phase after argan oil consumption. In conclusion, we show for the first time that consumption of argan oil may have an antiatherogenic effect by improving lipids, and the susceptibility of LDL to oxidation in type 2 diabetes patients with dyslipidemia, and can therefore be recommended in the nutritional management of type 2 diabetes.

Mutational heterogeneity in low-density lipoprotein receptor gene related to familial hypercholesterolemia in Morocco.

BACKGROUND: Familial hypercholesterolemia (FH) is an autosomal dominant disorder caused by mutations in the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB) and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. Until now, molecular data concerning FH in Morocco is still limited. To gain more information in this field and to assess the contribution of these three genes in the cause of FH determinism, we analyzed six unrelated Moroccan probands and twenty-five of their family's members. METHODS: After LDLR and APOB genotype analysis, we screened the LDLR gene for mutations using southern blot and PCR-sequencing analysis. We also screened the APOB gene for the two common mutations R3500Q and R3531C by PCR-mediated site-directed mutagenesis. The PCSK9 gene was analyzed by direct sequencing. RESULTS: We identified three novel mutations (C25X, IVS3+5G>T, D558A) and two mutations previously described (D151N, A480E) in the LDLR gene. The R3500Q and R3531C mutations are absent in our probands and for 1 proband, the implication of LDLR, APOB and PCSK9 genes was excluded, supporting the implication of a fourth gene in the determination of FH. CONCLUSION: These data are in agreement with our previous study that suggests a heterogeneous mutational spectrum of FH in Morocco.

Nutritional intervention study with argan oil in man: effects on lipids and apolipoproteins.

AIM: To evaluate whether the consumption of virgin argan oil (VAO) is associated with a change in serum lipids and reduces the risk of cardiovascular disease in healthy Moroccans. METHODS: Sixty volunteers consumed butter (25 g/day) during 2 weeks (stabilization period) and were randomly divided into two groups: the treatment group received 25 g/day of VAO during 3 weeks (intervention period), and the control group received 25 g/day of extra virgin olive oil (EVO). Throughout the study, weight, blood pressure, and daily food intake were measured. Serum total cholesterol and low- and high-density lipoprotein cholesterol, triglycerides, and apolipoproteins A-I and B were measured at the end of each diet period. RESULTS: Analysis of food intake showed that the daily diet is isocaloric for the butter regimen (2,537 +/- 244 kcal/day) as well as for the VAO and EVO regimens (2,561+/- 246 and 2,560 +/- 253 kcal/day, respectively). Analysis of the lipid intake showed a reduction in saturated fatty acids with VAO and EVO regimens (27 +/- 1.4 and 26.4 +/- 3.4%, respectively) as compared with the stabilization period (41.6 +/- 2.4%). The analysis of serum lipids showed a significant increase in high-density lipoprotein cholesterol and apolipoprotein A-I in both VAO group (8.4%, p = 0.012, and 5.2%, p = 0.027, respectively) and EVO group (17.3%, p = 0.001, and 5.9%, p = 0.036, respectively). However, low-density lipoprotein cholesterol and apolipoprotein B (13.8%, p = 0.037, and 7.8%, p = 0.039, respectively) decreased significantly only in EVO group as compared with the stabilization period, while triglycerides decreased significantly by 17.5% (p = 0.039) only in VAO group. CONCLUSION: These results confirm the cholesterol-lowering effect of EVO and show for the first time the triglyceride-lowering effect of VAO in men.

Probucol promotes reverse cholesterol transport in heterozygous familial hypercholesterolemia. Effects on apolipoprotein AI-containing lipoprotein particles.

In order to investigate the effect of Probucol therapy on reverse cholesterol transport, apo AI-containing lipoprotein particles were isolated and characterized, and their cholesterol effluxing capacity and LCAT activity were assayed in four familial hypercholesterolemia patients before and after 12 weeks of Probucol therapy. Four major subpopulations of apo A-containing lipoprotein particles are separated before and after drug treatment; LpAI, LpAI:AII, LpAIV, LpAI:AIV:AII. Probucol reduces both total plasma and LDL-cholesterol (-17 and -14%, respectively). Apo B decreases slightly (-7.6%). Plasma HDL-cholesterol and apo AI decrease by 36.6 and 34.7%. LpA-I showed a marked decrease (-46%). Moreover, plasma LCAT and CETP activities were markedly increased under Probucol treatment. Analysis of lipoprotein particles showed that Probucol induces a decrease of protein content and an increase of cholesterol and triglycerides contents. Interestingly, Probucol induces an enhancement of LCAT activity in LpAI (4.5-fold). This drug induces a trend toward greater cholesterol efflux from cholesterol-preloaded adipose cells promoted by Lp AI and Lp AIV but not by Lp AI:AII. This study confirms the hypothesis, in addition to the lowering LDL-cholesterol levels and antioxidant effects of Probucol, that HDL reduction was not an atherogenic change in HDL system but may cause an antiatherogenic action by accelerating cholesterol transport through HDL system, promoting reverse cholesterol transport from peripheral tissues.

Apolipoproteins and lipoprotein particles in Moroccan patients with previous myocardial infarction.

We investigated for the first time in the Moroccan population the relationship between lipoprotein particles and the progression of coronary atherosclerosis. Plasma lipid variables, including total cholesterol, triglycerides, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, apolipoproteins AI and B, Lp AI, Lp AI: AII, and Lp(a) were measured in 40 Moroccan adults who suffered a verified myocardial infarction before the age of 50 years. The results were compared with a healthy control group. Plasma total cholesterol, triglyceride, and Lp AI: AII levels of patients did not differ significantly from control subjects. Patients had lower plasma high-density lipoprotein-cholesterol (P < 0.05), apo AI (P < 0.05), and Lp AI (P < 0.001) than control subjects, suggesting that the cholesterol reverse transport system is altered in patients with previous myocardial infarction. However, patients had higher plasma low-density lipoprotein-cholesterol (P < 0.001), apo B (P < 0.001), and Lp(a) (P < 0.001). In all patients the best predictor of cardiovascular risk was the independent risk factor Lp(a) plasma level, and the Lp AI plasma level. In this study, the increased coronary atherosclerosis risk with elevated plasma levels of apo B and Lp(a), and with reduced Lp AI, was substantially modified by smoking habits, but not by family history of myocardial infarction.

The genetics of a small autosomal region of Drosophila melanogaster containing the structural gene for alcohol dehydrogenase. VII. Characterization of the region around the snail and cactus loci.

The genetic interval 35C to 36A on chromosome arm 2L of Drosophila melanogaster has been saturated for mutations with visible or lethal phenotypes. 38 loci have been characterized, including several maternal-effect lethals (vasa, Bic-C, chiffon, cactus and cornichon) and several early embryonic lethals, including snail and fizzy. About 130 deletions have been used to order these loci. Complex interactions between mutant alleles have been uncovered in the immediate genetic environs of the snail gene, as has further evidence for an interaction between this region and that including the nearby genes no-ocelli and elbow.

Mutant Drosophila embryos in which all cells adopt a neural fate.

In the Drosophila embryo, early developmental decisions lead to all cells adopting one of several initial fates, such as those characteristic of the germ layers. The central nervous system is formed subsequently from the neurogenic region of the ectoderm, in which progenitor cells of the neuroblasts and ventral epidermis are intermingled. Two classes of genes govern the segregation of neuroblasts and peripheral sensory organs. The pro-neural class of genes, for example, the achaete-scute complex, participates in the initial decision to make each uniquely positioned neuroblast or sensory organ, but are initially expressed in groups of cells. The segregation of a neuroblast or sensory organ from an equivalent group of equipotential cells involves a mechanism of lateral inhibition whereby the future epidermal cells are prevented from engaging in the primary dominant neural fate. In the absence of this inhibitory signal, all cells of the group will become neural by default. The neurogenic class of genes is thought to mediate these cell interactions. Here we report that cells in embryos mutant for shaggy which are unable to adopt any of the early initial fates, instead develop neural characteristics.

The twist gene: isolation of a Drosophila zygotic gene necessary for the establishment of dorsoventral pattern.

The twist zygotic gene appears to be involved in the establishment of the dorso-ventral pattern in Drosophila embryos. Homozygous twist embryos are partially dorsalized, their gastrulation is abnormal, and they fail to differentiate mesoderm. We determined the temperature-sensitive period of twist around the gastrulation time, and we isolated the gene. A 300 kb chromosomic walk allowed the detection of the 70 kb deletion that delimits the twist region in Df(2R)twiS60. Southern blot analyses of 21 EMS induced twist allele DNAs and systematic Northern blot analyses all over this 70 kb region lead to the localization of the twist gene: within about 10 kb at the left border of the deletion, 2 twist alleles show each a small deletion that uncover a transcription unit whose expression occurs about at the time of gastrulation.