PubMed Health⌕ Search

Biomedical subjects

Neusa Forti

Publications and source records attributed to Neusa Forti.

8 recordsLinked to original sources
PubMed2005

[Postprandial lipemia: influence of aging].

OBJECTIVE: To investigate the behavior of postprandial lipemia assessed by means of repeated measurements of triglyceride levels in healthy individuals aged from 20 to 50 years, divided into the following 3 age groups: GI--from 20 to 30 years; GII--from 31 to 40 years; and GIII--from 41 to 50 years. METHODS: Triglyceride levels were measured in 3 conditions: after a 12-hour fast, and 2 and 6 hours after a standard meal containing 40 g of fat. RESULTS: The repeated-measures analysis of triglyceride levels showed a distinct behavior of the age groups throughout the 6 hours. The younger participants (GI) had a reduction in the triglyceride levels in the sixth hour; the elderly (GIII) had increasing values in the sixth hour; and those in the intermediate age group (GII) maintained their triglyceride levels, when comparing the second and sixth hours of blood collection. The differences in behavior were significant (P=0.01). CONCLUSION: In a healthy adult population sample, aging influences the postprandial lipemia behavior.

Adult↗
PubMed2005

Lack of effect of captopril on the metabolism of an artificial lipid emulsion similar to chylomicrons in hypertensive hypercholesterolemic patients.

OBJECTIVE: To assess the effect of captopril, an angiotensin-converting enzyme inhibitor, on the metabolism of chylomicrons and their remnants and the possible alterations in the concentrations of plasma lipids caused by the drug in hypertensive hypercholesterolemic individuals. METHODS: The metabolism of chylomicrons was tested with the method of artificial lipid emulsion of chylomicrons labeled with 3H-cholesteryl oleate. The emulsion was injected intravenously in 10 patients with mild-moderate arterial hypertension before and 45 days after treatment with captopril (50 mg/day). After injection, blood samples were collected during 60 minutes at pre-established time intervals for determining the decay curve, the fractional catabolic rate (FCR in min-1), and the plasma residence time of the artificial lipid emulsion by analyzing different compartments. The plasma concentrations of the lipids were also assessed before and after treatment. RESULTS: The fractional catabolic rate (min-1) of the lipid emulsion before and after treatment with captopril (0.012 +/- 0.003 and 0.011 +/- 0.003, respectively; p = 0.85, n.s.) and the plasma residence time of the emulsion (83.3 +/- 20.8 and 90.9 +/- 22.5 min, n.s.) did not change, but the total cholesterol and LDL-C levels decreased by 7% and 10%, respectively (p = 0.02). The concentrations of HDL-C, triglycerides, Lp(a), and apolipoproteins AI and B did not change. CONCLUSION: Treatment with captopril, evaluated with the artificial lipid emulsion method, does not cause deleterious changes in the metabolism of chylomicrons and their remnants.

Antihypertensive Agents↗
PubMed2002

Molecular basis of familial hypercholesterolemia in Brazil: Identification of seven novel LDLR gene mutations.

Low-density lipoprotein receptor (LDLR) gene mutations cause familial hypercholesterol-emia (FH), one of the most common single gene disorders. The spectrum of LDLR mutations in Brazil is not known. The aim of this study was the characterization of LDLR mutations in 35 unrelated Brazilian patients with heterozygous FH. The promoter region, the 18 exons and the flanking intron sequences of the LDLR gene were screened by PCR-SSCP analysis and by DNA sequencing. In addition, we have screened the apolipoprotein B gene (APOB) for known mutations (R3500Q and R3531C) that cause Familial defective apo B-100 (FDB) by PCR-RFLP procedure. We found two nonsense (E92X and C371X) and six missense LDLR mutations (R236W, G322S, G352D, A370T, C675W and C677Y), that were previously described in FH patients from other populations. We also found five novel missense [G(-20)R, T476P, V503G, D580H and S652R] and two novel frame shift LDLR mutations (FsR757 and FsS828). Four patients were found to carry two different mutations in the LDLR gene: G352D and A370T (one patient), S652R and C675W (one patient) and T476P and V503G (two patients). APOB mutations were not found. These findings demonstrate that there is a broad spectrum of mutations in the LDLR gene in FH individuals from Brazil.

Adult↗
PubMed2002

A method to detect the G894T polymorphism of the NOS3 gene. Clinical validation in familial hypercholesterolemia.

An endothelial nitric oxide synthase gene (NOS3) polymorphism in exon 7 (G894T), resulting in Glu298Asp substitution at protein level, has been associated with myocardial infarction, hypertension and coronary atherosclerosis in some populations. This polymorphism is usually identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). However, the procedures described to date do not eliminate the possibility of misclassification and either require confirmation by DNA sequencing or are time-consuming. In this study, a PCR-RFLP procedure to detect the G894T polymorphism at the NOS3 was optimized by the introduction of a constitutive cleavage site in the amplification product. This cleavage site provides an internal control for enzymatic activity to avoid mistyping. The method was validated by the study of 35 white unrelated individuals with familial hypercholesterolemia and 70 controls. The frequency of the variant allele (T) was similar between both groups (27% vs. 22%, NS), and comparable to the frequency found in other white populations. However, future studies are necessary to confirm these data. In summary, the optimized procedure for detection of the G894T NOS3 polymorphism is rapid, simple, and does not require confirmatory tests. Using this method, we found no association between this polymorphism and familial hypercholesterolemia.

Adolescent↗
PubMedDate not supplied

[Risk factors for atherosclerosis in children and adolescents with family history of premature coronary artery disease].

OBJECTIVES: To identify the prevalence of dyslipidemia in a group of 109 children and adolescents with a family history of premature coronary artery disease and to investigate the association between dyslipidemia and other risk factors for atherosclerosis. METHODS: Total cholesterol, low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), triglycerides, body mass index, blood pressure, physical activity, smoking, per capita income and maternal schooling were investigated. RESULTS: Total cholesterol and LDL-C levels were higher than desirable in 27.5% and 19.3%, respectively, of our patients; 13.8% had lower HDL-C values and 13.0% presented hypertriglyceridemia. Obesity and excess weight were observed in 25.7% of the cases. Out of these, 57.1% had abnormal lipid values. Dyslipidemia was observed in 38.5%, either alone or in combination with other risk factors. Smoking was observed in 3.6%, hypertension in 2.7% and physical inactivity in 72.5%. There was no relationship between dyslipidemia and per capita income, maternal schooling and physical inactivity. However, obesity and excess weight were identified as significantly associated with the occurrence of dyslipidemia (p = 0.02; odds ratio = 2.82, 95% CI = 1.6-6.81). CONCLUSION: In children and adolescents with a family history of premature coronary artery disease, early identification of the risk factors for atherosclerosis is essential to allow the implementation of preventive measures.

Adolescent↗