| Autor: |
Tillander V; Division of Clinical Chemistry, Cardio Metabolic Unit, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden., Holmer M; Unit of Gastroenterology and Hepatology, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.; Division of Hepatology, Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden., Hagström H; Unit of Gastroenterology and Hepatology, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.; Division of Hepatology, Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden., Petersson S; Department of Clinical Science, Intervention and Technology, Division of Medical Imaging and Technology, Karolinska Institutet, Stockholm, Sweden.; Department of Medical Radiation Physics and Nuclear Medicine, Karolinska University Hospital, Stockholm, Sweden., Brismar TB; Department of Clinical Science, Intervention and Technology, Division of Medical Imaging and Technology, Karolinska Institutet, Stockholm, Sweden.; Department of Radiology, Karolinska University Hospital in Huddinge, Stockholm sE-14186, Sweden., Stål P; Unit of Gastroenterology and Hepatology, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.; Division of Hepatology, Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden., Lindqvist C; Unit of Gastroenterology and Hepatology, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.; Medical Unit Clinical Nutrition, Karolinska University Hospital, Stockholm, Sweden. |
| Abstrakt: |
Dietary fatty acids (FA) affect metabolic risk factors. The aim of this study was to explore if changes in dietary fat intake during energy restriction were associated with plasma FA composition. The study also investigated if these changes were associated with changes in liver fat, liver stiffness and plasma lipids among persons with non-alcoholic fatty liver disease. Dietary and plasma FA were investigated in patients with non-alcoholic fatty liver disease ( n 48) previously enrolled in a 12-week-long open-label randomised controlled trial comparing two energy-restricted diets: a low-carbohydrate high-fat diet and intermittent fasting diet (5:2), to a control group. Self-reported 3 d food diaries were used for FA intake, and plasma FA composition was analysed using GC. Liver fat content and stiffness were measured by MRI and transient elastography. Changes in intake of total FA ( r 0·41; P = 0·005), SFA ( r 0·38; P = 0·011) and MUFA ( r 0·42; P = 0·004) were associated with changes in liver stiffness. Changes in plasma SFA ( r 0·32; P = 0·032) and C16 : 1 n -7 ( r 0·33; P = 0·028) were positively associated with changes in liver fat, while total n -6 PUFA ( r -0·33; P = 0·028) and C20 : 4 n -6 ( r -0·42; P = 0·005) were inversely associated. Changes in dietary SFA, MUFA, cholesterol and C20:4 were positively associated with plasma total cholesterol and LDL-cholesterol. Modifying the composition of dietary fats during dietary interventions causes changes in the plasma FA profile in patients with non-alcoholic fatty liver disease. These changes are associated with changes in liver fat, stiffness, plasma cholesterol and TAG. Replacing SFA with PUFA may improve metabolic parameters in non-alcoholic fatty liver disease patients during weight loss treatment. |
