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ABSTRACT: In this study we evaluated the possible association between five single nucleotide polymorphisms in ABCG5 (rs6720173) and ABCG8 (rs11887534, rs4148211, rs4148217 and rs6544718) genes and ezetimibe response in Chilean hypercholesterolemic subjects. A total of 60 non-related hypercholesterolemic subjects, aged 18 to 65 years old were included in this study. These subjects were treated with ezetimibe (10mg/day) during one month. The ABCG5 and ABCG8 genotypes were assessed by PCR-RFLP. The genotype distribution of the ABCG5/ABCG8 polymorphisms was in Hardy-Weinberg equilibrium. Our results showed that the investigated polymorphisms were not associated with the response to ezetimibe. Nevertheless, the T allele of rs6544718 polymorphism was related to higher baseline levels of LDL-cholesterol (p<0.001). In addition, the G allele for the rs4148211 polymorphism was associated with greater baseline concentrations of triglycerides (P=0.019). This allele was also associated with lower concentrations of HDL-cholesterol (P=0.027), after ezetimibe treatment. Our results suggest that the studied polymorphisms do not affect the therapeutic response to ezetimibe in the evaluated subjects.
International Journal of Morphology 10/2012; 30(2):688-695. · 0.24 Impact Factor
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ABSTRACT: Statins are normally the first-line therapy for hypercholesterolemia (HC); however, the lipid-lowering response shows high interindividual variation. We investigated the effect of four polymorphisms in CYP3A4, CYP3A5 and ABCB1 genes on response to atorvastatin and CYP3A4 activity in Chilean subjects with HC.
A total of 142 hypercholesterolemic individuals underwent atorvastatin therapy (10mg/day/1month). Serum lipid levels before and after treatment were measured. Genetic variants in CYP3A4 (-290A>G, rs2740574), CYP3A5 (6986A>G, rs776746) and ABCB1 (2677G>A/T, rs2032582 and 3435C>T, rs1045642) were analyzed by PCR-RFLP. CYP3A4 enzyme activity in urine samples was assessed through determination of 6β-hydroxycortisol/cortisol free ratio (6βOHC/FC).
After 4weeks of therapy, a significant reduction in total cholesterol (TC) and LDL-c was observed (P<0.001). The G allele for -290A>G polymorphism was related to higher percentage of variation in TC and LDL-c (P<0.001). Moreover, same allele was associated with higher HDL-c variation (P=0.017). In addition, CYP3A4 enzyme activity was lower in subjects carrying this polymorphism (P=0.009). No differences were observed for CYP3A5 and ABCB1 variants.
Our results suggest that presence of G allele for -290A>G polymorphism determines a better response to atorvastatin, being also associated with lower CYP3A4 activity in vivo, causing an increased atorvastatin activity.
Clinica chimica acta; international journal of clinical chemistry 11/2011; 413(3-4):495-501. · 2.54 Impact Factor
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ABSTRACT: In the current study, we investigated the effect of propolis on diabetic mice undergoing propolis treatment (150 mg/kg/day) for a 6 week period. We also evaluated serum lipids, glucose, insulin levels and the effect on glucose uptake of 2-deoxy-D-[2,6-3H] glucose, [14C]-glycogen synthesis and [U-14C]-D-glucose decarboxylation induced by insulin in muscle tissue. Our results show that treatment with propolis (150 mg/kg/day) reduced insulin and HOMA index (P<0.05). Propolis also lowered abdominal obesity (P<0.05). No effects over serum glucose, total cholesterol and triglycerides levels were observed. We also observed that uptake of 2-deoxy-D-[2,6-3H] glucose, [14C]-glycogen synthesis and [U-14C]-D-glucose decarboxylation induced by insulin in soleus muscle of mice treated with propolis were significantly greater than control group (P<0.05). In summary, our data establishes that propolis modulates glucose metabolism. This result constitutes important data indicating that propolis can be used as a polyphenols source with antidiabetogenic activity.
International Journal of Morphology. 01/2011; 29(29):754-761.
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ABSTRACT: In the current study, we investigated the effect of propolis on diabetic mice undergoing propolis treatment (150 mg/kg/day) for a 6 week period. We also evaluated serum lipids, glucose, insulin levels and the effect on glucose uptake of 2-deoxy-D-[2,6-3H] glucose, [14C]-glycogen synthesis and [U-14C]-D-glucose decarboxylation induced by insulin in muscle tissue. Our results show that treatment with propolis (150 mg/kg/day) reduced insulin and HOMA index (P<0.05). Propolis also lowered abdominal obesity (P<0.05). No effects over serum glucose, total cholesterol and triglycerides levels were observed. We also observed that uptake of 2-deoxy-D-[2,6-3H] glucose, [14C]-glycogen synthesis and [U-14C]-D-glucose decarboxylation induced by insulin in soleus muscle of mice treated with propolis were significantly greater than control group (P<0.05). In summary, our data establishes that propolis modulates glucose metabolism. This result constitutes important data indicating that propolis can be used as a polyphenols source with antidiabetogenic activity.
International Journal of Morphology. 01/2011; 29(3-29):754-761.
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ABSTRACT: To investigate the possible association between the codon 72 polymorphism (Pro72Arg, rs1042522) of the tumor suppressor gene (TP53) and the presence of coronary artery disease (CAD) in Chilean subjects.
A total of 209 unrelated patients with a diagnosis of CAD confirmed by angiography (33-74 years old) and 216 healthy controls (30-68 years old) were included in this study. The Pro72Arg polymorphism of the TP53 gene was evaluated by PCR-RFLP.
The genotype distribution for the Pro72Arg variant of the TP53 gene in CAD patients (PP: n = 13, 6.2%; PR: n = 61, 29.4%; RR: n = 135, 64.6%) and controls (PP: n = 18, 8.3%; PR: n = 94, 43.5%; RR: n = 104, 48.1%) was significantly different (p = 0.003). Similarly, the allelic frequency was also different (p = 0.003). The odds ratio for CAD related to the 72Arg allele was 2.0 (95% CI = 1.33-2.90), confirming the presence of an association.
These findings suggest that the Pro72Arg polymorphism of the TP53 gene is associated with CAD in Chilean individuals.
Medical Principles and Practice 01/2011; 20(2):171-6. · 0.89 Impact Factor
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Revista Chilena de Cardiología. 29:201-206.
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Revista Chilena de Cardiología. 29:19-27.
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Revista Chilena de Cardiología. 29:214-220.
