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Biomedical subjects

M Feki

Publications and source records attributed to M Feki.

14 recordsLinked to original sources
PubMed2006

Apolipoprotein B signal peptide polymorphism: distribution and influence on lipid parameters in Tunisian population.

Apolipoprotein B (apo B) is the major protein component of LDL, VLDL and chylomicrons. Numerous polymorphisms of the apolipoprotein B gene have been described. Particularly, the insertion/deletion polymorphism located in the coding part of the signal peptide of apo B, associated with modification of lipid concentrations and the risk of cardiovascular disease, has been reported in the general population. No such study in the Tunisian population has been performed. The aim of our study was to assess the effect of insertion/deletion polymorphism of the apolipoprotein B gene on lipid levels in a sample of the Tunisian population. A total of 458 unrelated subjects (321 men and 137 women) were included. The insertion/deletion polymorphism was determined by electrophoresis on polyacrylamide gels after PCR amplification. The relative frequencies of the Ins and Del alleles were 0.74 and 0.26, respectively. These frequencies were similar to those found in other Caucasian populations. There was no significant difference in serum TC, TG, and HDL-C levels due to the influence of the genotypes. However, significant variation among the three genotypes was seen for LDL-cholesterol (p<0.001) and apo B (p<0.001) levels. Individuals homozygous for the Del allele had higher levels than individuals homozygous for the Ins allele, while individuals heterozygous for both alleles exhibited intermediate levels. When the data were analyzed in men and women separately, a similar effect was seen in both groups. Our results show that distribution of apo B insertion/deletion polymorphism in Tunisians is similar to other Caucasian population and confirm the reported association with serum LDL-cholesterol and apo B concentrations.

Adult↗
PubMed2006

Apolipoprotein E polymorphism in the Tunisian population: frequency and effect on lipid parameters.

OBJECTIVES: We determined the frequencies of apolipoprotein E (apo E) gene alleles and examined the association between apo E polymorphism and lipid parameters in a sample of the Tunisian population. DESIGN AND METHODS: Apo E polymorphism was investigated using PCR, and plasma lipid parameters were measured in 122 men and 111 women aged 35 to 87 years. RESULTS: The allele frequencies were epsilon2: 7.3%, epsilon3: 84.6%, and epsilon4: 8.1%. Apo E polymorphism was associated with significant differences (P<0.001) in total cholesterol, apo B and LDL cholesterol in both men and women. epsilon2 carriers had the lowest mean total cholesterol, apo B and LDL-C concentrations, and subjects with the epsilon4 allele had the highest levels. Triglycerides levels increased with the epsilon4 allele, but this did not reach statistical significance. These results remained unchanged after adjustment for age, body mass index, sex, hypertension, diabetes and smoking. However, in obese subjects (BMI>30 kg/m2), TG concentrations were significantly lower in individuals homozygous for the epsilon3 allele compared to those with the alleles epsilon2 or epsilon4. CONCLUSION: In this sample of the Tunisian population, the distribution of apo E gene alleles is similar to that observed in Southern European populations with low prevalence of the epsilon4 allele. Variations in the apo E gene play a role in determining plasma lipid levels. These data also suggest that effects of apo E alleles on lipids levels are partly dependent on environmental variables such as BMI. These findings highlight the importance of the gene/environment interaction on the deleterious effect of obesity on cardiovascular risk factors.

Adult↗
PubMed2006

Association between dietary fat and antioxidant status of Tunisian type 2 diabetic patients.

BACKGROUND: The antioxidant enzymes: superoxide dismutase (Cu/Zn SOD) and glutathione peroxidase (GSH-Px) provide a defense against the damage of cells by reactive oxygen species, which increased in diabetic state. It was demonstrated that dietary treatment could improve the antioxidant status in patients with type 2 diabetes mellitus. This study was undertaken to determine if erythrocyte Cu/Zn SOD and GSH-Px activities correlate with dietary nutrients in 35 selected type 2 diabetic patients (21 women and 14 men) without diabetic complications. RESULTS: We found that erythrocyte Cu/Zn SOD was diminished in patients with poor controlled diabetes and GSH-Px activity was significantly decreased in obese compared with non-obese type 2 diabetic patients (1.07+/-0.87 and 2.36+/-1.99 U/ml, respectively; P=0.024). Both erythrocyte Cu/Zn SOD and GSH-Px activities were positively correlated to erythrocyte omega3-polyunsaturated fatty acids (PUFA). In non-obese diabetic patients, only GSH-Px activity was correlated negatively to the fraction of linoleic acid (18:2omega6) and arachidonic acid (20:4omega6) in erythrocytes phospholipids. CONCLUSIONS: The data of this study reveal that activities of erythrocyte antioxidant enzymes were altered in type 2 diabetic patients. Further studies are needed to determine if diet supplemented with omega3-PUFA is required to improve antioxidant defense system in diabetic state.

Adiposity↗
PubMed2006

[Homocysteinemia and coronary artery disease: a case-control study in a Tunisian population].

We have determined the prevalence of hyperhomocysteinemia and tested its relationship with coronary heart disease in Tunisian patients. The study included 70 angiogrphically proven coronary patients and 140 age- and sex-matched healthy subjects. Plasma homocysteine folate and vitamin B12 were analyzed by immunoenzymatic methods. Hyperhomocysteinemia was considered for plasma homocysteine concentration >17 micromol/L. Mean plasma homocysteine concentration and hyperhomocysteinemia prevalence were significantly (p<0.001) higher in patients (16.3 +/- 7.9 micromol/L and 29%) than controls (12.6 +/- 4.0 micromol/L and 10%). The association between hyperhomocysteinemia and coronary heart disease persisted after adjusting on main cardiovascular risk factors (multi adjusted odds ratio, 2.99; 95% CI, 1.18-7.59; p=0.02). No association was observed between hyperhomocysteinemia and coronary disease severity and extent. This study showed an independent association between hyperhomocysteinemia and coronary heart disease, suggesting a role of hyperhomocysteinemia in atherothrombogenesis. However, causal relationship is not yet established. Until results of homocysteine-lowering therapy trials become available, hyperhomocysteinemia should be researched and treated in coronary heart disease patients.

Case-Control Studies↗
PubMed2004

Vitamin D deficiency in Tunisia.

This study seeks to estimate the status of serum 25-hydroxyvitamin D [25(OH)D] in a healthy section of the population in Tunisia and to compare the achieved results with other published data. A transverse descriptive inquiry was carried out between January and March 2002. Three hundred and eighty-nine subjects aged 20-60 years were included in the study. A questionnaire was used to investigate clinical characteristics: sunlight exposure to ultraviolet light and, for women, parity, breast feeding, whether or not they wore the veil, and menopause. A dietary investigation estimated calcium and vitamin D intake. Morning fasting blood was collected from each subject for the measurement of the following parameters: serum calcium, phosphorus, albumin, alkaline phosphatase, 25(OH)D, parathyroid hormone (PTH). Hypovitaminosis D was defined by a cut-off of 37.5 nmol/l. The population studied was largely female, for the greater part housewives. The accumulated prevalence of hypovitaminosis D was 47.6%, increasing with age. Hypovitaminosis is highly prevalent in women (P<0.001). Multiparity, menopause, wearing the veil, and calcium and vitamin D dietary intake are factors associated with hypovitaminosis D (P<0.05). Analysis of logistic regression shows that only multiparity and vitamin D dietary intake are independent predictive factors. The status of serum 25(OH)D in Tunisia resembles that in southern European countries rather than in Middle Eastern countries. Insufficient vitamin D diet intake, higher parity and wearing the veil explain this deficiency in Tunisia. Dietary enrichment or supplementation by vitamin D and a more outdoor lifestyle, especially for older people, should be seriously considered as a way to reduce this deficiency in Tunisia.

Adult↗
PubMed2001

Prolactin levels in Behçet's disease: no correlation with disease manifestations and activity.

OBJECTIVE: To assess prolactin level and its possible role in the pathogenesis and disease expression of patients with Behçet's disease (BD). MATERIALS AND METHODS: Twenty-eight patients with the diagnosis of Behçet's disease were selected. They all fulfilled the international criteria for BD. The control group consisted of 17 males and 6 females. Patients are divided into subgroups according to the clinical and paraclinical characteristics such as disease duration, ocular, articular and neurological involvement. Serum prolactin was measured by ELISA using Merck Kits on a Maggia 7000 Analyser. The normal range in males was<17ng/ml in males and<18ng/ml in females. The mean PRL level in each group and subgroup was calculated and compared with Student's t test. RESULTS: The mean prolactin level in the BD group (mean=13.76, SD=6.82), was higher than in the control group (mean=10.13, SD=5.46) with no statistically significant difference. The mean prolactin levels in all subgroups of patients with BD were higher than normal, but no statistically significant difference was shown between these subgroups. CONCLUSION: Hyperprolactinemia occurred in a small number of patients with BD and its significance remained unclear. Serum PRL level did not correlate with disease manifestations and activity.

Adolescent↗
PubMed2001

[Vitamin E: structure, metabolism, and functions].

Vitamin E is a generic term denoting eight different isomers among which alpha-tocopherol is the most important and most active. Vitamin E metabolism is closely linked to lipids during intestinal absorption, plasma secretion and transport, and tissue uptake. It is a key compound involved in many physiological processes, such as neurological and immune functions. The most common role of vitamin E is its antioxidant effect, protecting molecules and tissues against the deleterious effect of free radicals. Vitamin E also contributes to the stabilization of biological membranes. In addition, it intervenes in the regulation of several enzymes and probably has impact on gene expression. Advancing knowledge about vitamin E has been achieved with high performance liquid chromatography, making assay accessible to many laboratories, and the use of deuterated derivatives to better apprehend its metabolism. Certain issues remain unresolved concerning the molecular basis of vitamin E's mechanism of action and the exact nature of metabolic dysfunction leading to the clinical manifestations of severe vitamin E deficiency.

Humans↗
PubMed2001

[Vitamin E deficiency. Etiopathogenesis, clinical, histopathologic, and electrical features, and main etiologies].

Vitamin E deficiency is frequently observed in human pathology. In most cases, deficiency is moderate and asymptomatic. Severe deficiency is rare and presents as a progressive neurological syndrome including cerebellar ataxia and posterior cord injury. Neuropathological and electrophysiological features confirm spinocerebellar degeneration. The pathophysiology of vitamin E deficiency nervous dysfunction is still unknown. Oxidative alterations due to the lack of the main lipid-soluble antioxidant could be involved. A few causes of vitamin E deficiency are recognized (malnutrition, impaired lipid absorption, specific anomaly of hepatic or intestinal secretion of vitamin E, excessive endogenous consumption), but diseases associated with vitamin E deficiency are numerous and divers. Symptomatic severe deficiency is constantly observed in ataxia with vitamin E deficiency and abetalipoproteinemia. Intestinal, hepatobiliary, and pancreatic diseases are often associated with more or less marked deficiency. Other pathological circumstances such as malnutrition, alcoholism, hemolytic anemia, renal failure and hemodialysis could be associated with moderated and asymptomatic vitamin E deficiency. Oral or regular administration of high-dose vitamin E is required for patients with symptomatic severe deficiency. An adapted supplementation is recommended for patients with a marginal vitamin E status.

Electrophysiology↗
PubMed2001

[Vitamin E deficiency: risk factor in human disease?].

Oxidative stress is suspected to intervene in certain chronic diseases. Much research has been devoted to the relationship between vitamin E, a major lipid-soluble antioxidant, and certain widespread diseases. Experimental and epidemiological proof supports a protective effect of vitamin E in a number of pathological processes such as coronary heart disease, cancer, cataract, diabetes mellitus, and Alzheimer disease. Randomized clinical trials have not confirmed a beneficial effect of vitamin E supplementation on the progression of these diseases. Certain methodological biases could however have affected these studies, explaining conflicting results. These biases include inaccuracy of vitamin E intake estimates and changes in eating habits during the course of the survey. An insufficient supplementation period using an insufficient dose and inclusion of aged and high-risk patients are the main limitations of the reported clinical trials. Large scale randomized clinical trials including healthy and low-risk subjects, along with prolonged administration of high-dose natural vitamin E, associated with synergetic compounds, and testing on morphological or biological features, will allow a better understanding of the relationship between vitamin E and chronic diseases.

Cardiovascular Diseases↗
PubMed2000

Vitamin E and coronary heart disease in Tunisians.

BACKGROUND: Vitamin E (VE) is thought to be effective in preventing atherosclerosis. However, to date no consistent relationship has been identified between VE and coronary heart disease (CHD). This study was designed to assess the degree of association between VE and CHD in a sample of the Tunisian population. METHODS: Sixty-two angiographically confirmed coronary atherosclerotic patients and 65 age- and sex-matched controls were included. VE was measured in plasma and in the LDL fraction by HPLC. Cholesterol, triglycerides, and phospholipids were measured by enzymatic methods. RESULTS: A trend toward a meaningful decrease of plasma VE was observed in affected patients compared with controls (P: = 0.06). VE concentrations standardized for cholesterol and lipid concentrations were significantly lower (P: <0.02) in coronary patients than in controls (4.35 +/- 1.03 vs 4.82 +/- 1.23 mmol/mol for cholesterol-adjusted VE and 2.35 +/- 0.56 vs 2.66 +/- 0.65 mmol/mol for lipid-adjusted VE, respectively). In the LDL fraction, only cholesterol-standardized VE was significantly lower in cases than controls (3.84 +/- 1.13 vs 4.41 +/- 1.16 mmol/mol). This association between VE and CHD remained unchanged independent of age, sex, smoking habit, hypertension, and diabetes. In CHD patients, lower lipid-adjusted VE was associated with enhanced LDL susceptibility to oxidation but without alteration of the serum fatty acid profile. CONCLUSIONS: These results support the hypothesis that VE plays a role in preventing atherosclerosis.

Adult↗
PubMed1998

[Reference values of urinary orotic acid in a healthy Tunisian population].

BACKGROUND: Orotic acid (OA) is an intermediary metabolite of pyrimidine synthesis. An elevation of urinary orotic acid excretion has been described in congenital defect of the urea cycle enzymes and in primary orotic aciduria. Several techniques have been used to measure OA and many reference values are published without considering age and sex. POPULATION AND METHODS: The reference values of urinary OA excretion, expressed in mumol/mmol of creatinine, are reported in a healthy Tunisan population using a colorimetric method. The study included 20 men and 20 women (age = 31 +/- 11 years) and 30 children aged from 3 days to 8 years. RESULTS: There was a significant increase (P < 0.01) of urinary OA excretion in women (4.38 +/- 1.35) compared to men (3.26 +/- 0.80) and of children (5.03 +/- 1.14) compared to adults (3.82 +/- 1.24). Urinary OA excretion was significantly higher among children aged less than 1 year compared to older children. CONCLUSION: It is necessary for every laboratory practicing this kind of exploration to have its own norms which depend on both age and sex.

Adult↗
PubMed1998

Electrophysiology and nerve biopsy: comparative study in Friedreich's ataxia and Friedreich's ataxia phenotype with vitamin E deficiency.

The authors report a comparative study of peripheral nerve conductions and nerve biopsy and somatosensory evoked potentials between 15 patients with Friedreich's ataxia and 15 patients with Friedreich's ataxia phenotype with selective vitamin E deficiency. The patients in the two groups are of similar age, age of onset, and clinical phenotype. Peripheral motor nerve action potential amplitude, and conduction velocities are within normal ranges in the two groups. In the Friedreich's ataxia group there is an early and severe peripheral sensory axonal neuronopathy, characterised by an important reduction of the amplitude of sensory action potential, and important loss of myelinated fibres with complete disappearance of large myelinated fibres without any regenerative process. In the Friedreich's ataxia phenotype with selective vitamin E deficiency group there is slight-to-moderate axonal sensory neuropathy with normal to moderate decrease of large myelinated fibre density and important regeneration in nerve biopsy. Somatosensory evoked potentials are markedly involved in the two groups asserting a severe involvement of somatosensory pathway in lumbar, thoracic and cervical spinal cord. These findings suggest that the pathological mechanism involved in the two diseases are different: central peripheral axonopathy in Friedreich's ataxia and central distal axonopathy in Friedreich's ataxia phenotype with selective vitamin E deficiency.

Adult↗
PubMedDate not supplied

[Iron metabolism, overview and recent insights].

The paper is an up to date overview of knowledge on iron metabolism that integrate recent findings in this field. Significant advances were made in understanding the implication of protein factors (transporters, enzymes and regulation factors) in iron metabolism, as well as related genetic abnormalities. The research highlighted the complexity of mechanisms in charge of maintaining equilibrium of Fe in the body. The iron is vital to the life of cells, but its presence in excess is rather toxic. Iron is mostly required for hemoglobin synthesis. It is recycled between reticulo-endothelial macrophages and bone marrow that is the main user of iron. Intestinal absorption is a key step in determining iron capital in the body. Its rate is tightly controlled by several factors that act under influence of signals of unknown nature, which indicate iron needs and storage. The IRP/IRE (iron regulatory protein/iron responsive element) system controls cellular uptake, stores and exportation of iron, and heme synthesis. Mitochondrion is a dynamo of iron metabolism, being vital for heme synthesis and iron sulphur cluster genesis. The recent discovery of several mitochondrial proteins involved in iron metabolism resulted in better understanding mitochondrial iron movement, storage and exchange. Nevertheless, much remains to be known on the role of some actors such as HFE protein, hepcidin, hemojuvelin and transferrin receptor 2, and to determine the nature and mechanisms of signals regulating iron level in the body.

Biological Transport↗