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Human plasma lipid modulation in schistosomiasis mansoni depends on apolipoprotein E polymorphism.


ABSTRACT: Schistosomiasis mansoni is a parasitic liver disease, which causes several metabolic disturbances. Here, we evaluate the influence of Apolipoprotein E (APOE) gene polymorphism, a known modulator of lipid metabolism, on plasma lipid levels in patients with hepatosplenic schistosomiasis.Blood samples were used for APOE genotyping and to measure total cholesterol (TC), LDL-C, HDL-C and triglycerides. Schistosomiasis patients had reduced TC, LDL-C and triglycerides (25%, 38% and 32% lower, respectively; P<0.0001) compared to control individuals, whereas HDL-C was increased (10% higher; P?=?0.0136). Frequency of the common alleles, ?2, ?3 and ?4, was similar (P?=?0.3568) between controls (n?=?108) and patients (n?=?84), implying that APOE genotype did not affect susceptibility to the advanced stage of schistosomiasis. Nevertheless, while patient TC and LDL-C levels were significantly reduced for each allele (except TC in ?2 patients), changes in HDL-C and triglycerides were noted only for the less common ?2 and ?4 alleles. The most striking finding, however, was that accepted regulation of plasma lipid levels by APOE genotype was disrupted by schistosomiasis. Thus, while ?2 controls had higher TC and LDL-C than ?3 carriers, these parameters were lower in ?2 versus ?3 patients. Similarly, the inverse relationship of TG levels in controls (?2>?3>?4) was absent in patients (?2 or ?4>?3), and the increase in HDL-C of ?2 or ?4 patients compared to ?3 patients was not seen in the control groups.We confirm that human schistosomiasis causes dyslipidemia and report for the first time that certain changes in plasma lipid and lipoprotein levels depend on APOE gene polymorphism. Importantly, we also concluded that S. mansoni disrupts the expected regulation of plasma lipids by the different ApoE isoforms. This finding suggests ways to identify new metabolic pathways affected by schistosomiasis and also potential molecular targets to treat associated morbidities.

SUBMITTER: Martins da Fonseca CS 

PROVIDER: S-EPMC4106763 | BioStudies | 2014-01-01

REPOSITORIES: biostudies

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