Irene Cantero1, Itziar Abete1, Nancy Babio2, Fernando Arós3, Dolores Corella4, Ramón Estruch5, Montse Fitó6, James R Hebert7, M Ángel Martínez-González8, Xavier Pintó9, M Puy Portillo3, Miguel Ruiz-Canela8, Nitin Shivappa7, Julia Wärnberg10, Enrique Gómez-Gracia11, J Antoni Tur12, Jordi Salas-Salvadó2, M Angeles Zulet13, J Alfredo Martínez14. 1. Department of Nutrition, Food Science and Physiology, Center for Nutrition Research (CIN), Universidad de Navarra, Spain. 2. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Human Nutrition Department, Hospital Universitari Sant Joan, Institut d'Investigació Sanitaria Pere Virgili, Universitat Rovira i Virgili, Spain. 3. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Department of Cardiology, University Hospital Araba, Spain. 4. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Department of Preventive Medicine, University of Valencia, Spain. 5. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Department of Internal Medicine, Institut d'Investigacions Biomèdiques August Pi I Sunyer, Hospital Clinic, University of Barcelona, Spain. 6. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Cardiovascular and Nutrition Research Group, Institut de Recerca Hospital del Mar, Barcelona, Spain. 7. Cancer Prevention and Control Program, University of South Carolina, Columbia, SC 29208, USA. 8. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Departamento de Medicina Preventiva y Salud Pública, Universidad de Navarra, Navarra Institute for Health Research, Spain. 9. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Lipids and Vascular Risk Unit, Internal Medicine, Hospital Universitario de Bellvitge-IDIBELL-UB, Hospitalet de Llobregat, Spain. 10. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Department of Preventive Medicine, University of Malaga, Spain. 11. Department of Preventive Medicine, University of Malaga, Spain. 12. Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Research Group on Community Nutrition and Oxidative Stress, Universitat de les Illes Balears, Spain. 13. Department of Nutrition, Food Science and Physiology, Center for Nutrition Research (CIN), Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain. Electronic address: mazulet@unav.es. 14. Department of Nutrition, Food Science and Physiology, Center for Nutrition Research (CIN), Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain.
Abstract
BACKGROUND & AIMS: To assess the possible association between a validated Dietary Inflammatory Index (DII) and specific dietary components with suitable non-invasive markers of liver status in overweight and obese subjects within the PREDIMED study. METHODS: A cross-sectional study encompassing 794 randomized overweight and obese participants (mean ±SD age: 67.0 ± 5.0 y, 55% females) from the PREDIMED (PREvención con DIeta MEDiterránea) trial was conducted. DII is a validated tool evaluating the effect of diet on six inflammatory biomarkers (IL-1b, IL-4, IL-6, IL-10, TNF-α and C-reactive protein). Furthermore, a validated 137-item food-frequency-questionnaire was used to obtain the information about the food intake. In addition, anthropometric measurements and several non-invasive markers of liver status were assessed and the Fatty Liver Index (FLI) score was calculated. RESULTS: A higher DII and lower adherence to Mediterranean diet (MeDiet) were associated with a higher degree of liver damage (FLI > 60) in obese as compared to overweight participants. Furthermore, the DII score was positively associated with relevant non-invasive liver markers (ALT, AST, GGT and FLI) and directly affected FLI values. Interestingly, a positive correlation was observed between liver damage (>50th percentile FLI) and nutrients and foods linked to a pro-inflammatory dietary pattern. CONCLUSIONS: This study reinforced the concept that obesity is associated with liver damage and revealed that the consumption of a pro-inflammatory dietary pattern might contribute to obesity and fatty liver disease features. These data suggest that a well-designed precision diet including putative anti-inflammatory components could specifically prevent and ameliorate non-alcoholic fatty liver manifestations in addition to obesity.
RCT Entities:
BACKGROUND & AIMS: To assess the possible association between a validated Dietary Inflammatory Index (DII) and specific dietary components with suitable non-invasive markers of liver status in overweight and obese subjects within the PREDIMED study. METHODS: A cross-sectional study encompassing 794 randomized overweight and obeseparticipants (mean ± SD age: 67.0 ± 5.0 y, 55% females) from the PREDIMED (PREvención con DIeta MEDiterránea) trial was conducted. DII is a validated tool evaluating the effect of diet on six inflammatory biomarkers (IL-1b, IL-4, IL-6, IL-10, TNF-α and C-reactive protein). Furthermore, a validated 137-item food-frequency-questionnaire was used to obtain the information about the food intake. In addition, anthropometric measurements and several non-invasive markers of liver status were assessed and the Fatty Liver Index (FLI) score was calculated. RESULTS: A higher DII and lower adherence to Mediterranean diet (MeDiet) were associated with a higher degree of liver damage (FLI > 60) in obese as compared to overweight participants. Furthermore, the DII score was positively associated with relevant non-invasive liver markers (ALT, AST, GGT and FLI) and directly affected FLI values. Interestingly, a positive correlation was observed between liver damage (>50th percentile FLI) and nutrients and foods linked to a pro-inflammatory dietary pattern. CONCLUSIONS: This study reinforced the concept that obesity is associated with liver damage and revealed that the consumption of a pro-inflammatory dietary pattern might contribute to obesity and fatty liver disease features. These data suggest that a well-designed precision diet including putative anti-inflammatory components could specifically prevent and ameliorate non-alcoholic fatty liver manifestations in addition to obesity.
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