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Human plasma lipid modulation in schistosomiasis mansoni depends on apolipoprotein E polymorphism
Caíque Silveira Martins da Fonseca1, Adenor Almeida Pimenta Filho1, Bianka Santana dos Santos1
1Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Pernambuco (UFPE), Recife, Brazil.
Schistosomiasis causes dyslipidemia, altering lipid levels differently based on Apolipoprotein E (APOE) gene variants. This parasitic infection disrupts normal APOE regulation of plasma lipids, suggesting new therapeutic targets.
Area of Science:
- Genetics
- Metabolic Diseases
- Parasitology
Background:
- Schistosomiasis mansoni is a parasitic liver disease causing metabolic disturbances.
- Apolipoprotein E (APOE) gene polymorphism influences lipid metabolism.
Purpose of the Study:
- To evaluate the influence of APOE gene polymorphism on plasma lipid levels in patients with hepatosplenic schistosomiasis.
- To investigate how schistosomiasis affects APOE's regulation of lipid metabolism.
Main Methods:
- APOE genotyping was performed on blood samples.
- Plasma levels of total cholesterol (TC), LDL-C, HDL-C, and triglycerides were measured.
- Lipid levels and APOE allele frequencies were compared between schistosomiasis patients and controls.
Main Results:
- Schistosomiasis patients exhibited lower TC, LDL-C, and triglycerides, and higher HDL-C compared to controls.
- APOE allele frequencies were similar between patients and controls, indicating no effect on schistosomiasis susceptibility.
- Schistosomiasis disrupted the typical regulation of plasma lipids by APOE genotype, with altered lipid profiles observed in patients compared to controls for specific APOE alleles.
Conclusions:
- Schistosomiasis induces dyslipidemia.
- Plasma lipid and lipoprotein level alterations in schistosomiasis are influenced by APOE gene polymorphism.
- Schistosomiasis disrupts APOE's normal regulation of plasma lipids, highlighting potential new metabolic pathways and therapeutic targets.
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