Virginia Esteve-Luque1,2,3, Ariadna Padró-Miquel2,4,5, Marta Fanlo-Maresma1,2,3, Emili Corbella1,2,5, Xavier Corbella1,2,6, Xavier Pintó1,2,5,7, Beatriz Candás-Estébanez2,4,5,8. 1. Cardiovascular Risk Unit, Internal Medicine Department, Hospital Universitari de Bellvitge, 08907 L'Hospitalet de Llobregat, Spain. 2. Bellvitge Biomedical Research Institute (IDIBELL), 08908 L'Hospitalet de Llobregat, Spain. 3. Medicine and Translational Research, University of Medicine, Universitat de Barcelona, 08036 Barcelona, Spain. 4. Clinical Laboratory, Hospital Universitari de Bellvitge, 08907 L'Hospitalet de Llobregat, Spain. 5. CIBEROBN Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, 28029 Madrid, Spain. 6. School of Medicine, Universitat Internacional de Catalunya, 08017 Barcelona, Spain. 7. School of Medicine, Universitat de Barcelona, 08907 Barcelona, Spain. 8. Clinical Biochemistry, SCIAS-Hospital de Barcelona, 08034 Barcelona, Spain.
Abstract
BACKGROUND: Lipid metabolism disorders, especially hypertriglyceridemia (HTG), are risk factors for non-alcoholic fatty liver disease (NAFLD). However, the association between genetic factors related to HTG and the risk of NAFLD has been scarcely studied. METHODS: A total of 185 subjects with moderate HTG were prospectively included. We investigated the association between genetic factors' (five allelic variants with polygenic hypertriglyceridemia) clinical and biochemical biomarkers with NAFLD severity. The five allelic variants' related clinical and biochemical data of HTG were studied in all the subjects. NAFLD was assessed by abdominal ultrasound and patients were divided into two groups, one with no or mild NAFLD and another with moderate/severe NAFLD. RESULTS: Patients with moderate/severe NAFLD had higher weight and waist values and a higher prevalence of insulin resistance than patients with no or mild NAFLD. Moderate/severe NAFLD was independently associated with APOA5 rs3134406 and ZPR1 rs964184 variants, and also showed a significant inverse relationship with lipoprotein(a) [Lp(a)] concentrations. CONCLUSIONS: APOA5 rs3135506 and ZPR1 rs964184 variants and lipoprotein(a) are associated with moderate/severe NAFLD. This association was independent of body weight, insulin resistance, and other factors related to NAFLD.
BACKGROUND:Lipid metabolism disorders, especially hypertriglyceridemia (HTG), are risk factors for non-alcoholic fatty liver disease (NAFLD). However, the association between genetic factors related to HTG and the risk of NAFLD has been scarcely studied. METHODS: A total of 185 subjects with moderate HTG were prospectively included. We investigated the association between genetic factors' (five allelic variants with polygenic hypertriglyceridemia) clinical and biochemical biomarkers with NAFLD severity. The five allelic variants' related clinical and biochemical data of HTG were studied in all the subjects. NAFLD was assessed by abdominal ultrasound and patients were divided into two groups, one with no or mild NAFLD and another with moderate/severe NAFLD. RESULTS:Patients with moderate/severe NAFLD had higher weight and waist values and a higher prevalence of insulin resistance than patients with no or mild NAFLD. Moderate/severe NAFLD was independently associated with APOA5rs3134406 and ZPR1rs964184 variants, and also showed a significant inverse relationship with lipoprotein(a) [Lp(a)] concentrations. CONCLUSIONS:APOA5rs3135506 and ZPR1rs964184 variants and lipoprotein(a) are associated with moderate/severe NAFLD. This association was independent of body weight, insulin resistance, and other factors related to NAFLD.
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