Marjukka Kolehmainen1, Stine M Ulven1, Jussi Paananen1, Vanessa de Mello1, Ursula Schwab1, Carsten Carlberg1, Mari Myhrstad1, Jussi Pihlajamäki1, Elisabeth Dungner1, Eva Sjölin1, Ingibjörg Gunnarsdottir1, Lieselotte Cloetens1, Mona Landin-Olsson1, Björn Akesson1, Fredrik Rosqvist1, Janne Hukkanen1, Karl-Heinz Herzig1, Lars O Dragsted1, Markku J Savolainen1, Lea Brader1, Kjeld Hermansen1, Ulf Risérus1, Inga Thorsdottir1, Kaisa S Poutanen1, Matti Uusitupa1, Peter Arner1, Ingrid Dahlman1. 1. From the Institute of Public Health and Clinical Nutrition (MK, J Paananen, VdM, US, J Pihlajamäki, KSP, and MU) and the Institute of Biomedicine (CC), University of Eastern Finland, Kuopio, Finland; the Institute of Clinical Medicine, Clinical Nutrition (US and J Pihlajamäki) and Research Unit (MU), Kuopio University Hospital, Kuopio, Finland; the Department of Health, Nutrition and Management, Faculty of Health Sciences, Oslo, Norway, and Akershus University College of Applied Sciences, Oslo, Norway (SMU and MM); the Department of Medicine (H7), Karolinska Institute, Stockholm, Sweden (ID, PA, ED, and ES); the Unit for Nutrition Research, University of Iceland and Landspitali-The National University Hospital of Iceland, Reykjavik, Iceland (IG and IT); Biomedical Nutrition, Pure and Applied Biochemistry, Lund University, Lund, Sweden (LC and BÅ); the Departments of Endocrinology (ML-O) and Clinical Nutrition (BÅ), Skåne University Hospital, Lund, Sweden; the Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism, Uppsala University, Uppsala, Sweden (FR and UR); the Institute of Clinical Medicine, Department of Internal Medicine and Biocenter Oulu, University of Oulu, and Medical Research Center, Oulu University Hospital, Oulu, Finland (MJS and JH); University of Copenhagen, Faculty of Science, Department of Human Nutrition, Copenhagen, Denmark (LOD); Institute of Biomedicine, University of Oulu, Oulu, Finland (K-HH); the Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark (KH and LB); and VTT Technical Research Centre of Finland, Espoo, Finland (KSP).
Abstract
BACKGROUND: Previously, a healthy Nordic diet (ND) has been shown to have beneficial health effects close to those of Mediterranean diets. OBJECTIVE: The objective was to explore whether the ND has an impact on gene expression in abdominal subcutaneous adipose tissue (SAT) and whether changes in gene expression are associated with clinical and biochemical effects. DESIGN:Obese adults with features of the metabolic syndrome underwent an 18- to 24-wk randomized intervention study comparing the ND with the control diet (CD) (the SYSDIET study, carried out within Nordic Centre of Excellence of the Systems Biology in Controlled Dietary Interventions and Cohort Studies). The present study included participants from 3 Nordic SYSDIET centers [Kuopio (n = 20), Lund (n = 18), and Oulu (n = 18)] with a maximum weight change of ±4 kg, highly sensitive C-reactive protein concentration <10 mg/L at the beginning and the end of the intervention, and baseline body mass index (in kg/m²) <38. SAT biopsy specimens were obtained before and after the intervention and subjected to global transcriptome analysis with Gene 1.1 ST Arrays (Affymetrix). RESULTS: Altogether, 128 genes were differentially expressed in SAT between the ND and CD (nominal P < 0.01; false discovery rate, 25%). These genes were overrepresented in pathways related to immune response (adjusted P = 0.0076), resulting mainly from slightly decreased expression in the ND and increased expression in the CD. Immune-related pathways included leukocyte trafficking and macrophage recruitment (e.g., interferon regulatory factor 1, CD97), adaptive immune response (interleukin32, interleukin 6 receptor), and reactive oxygen species (neutrophil cytosolic factor 1). Interestingly, the regulatory region of the 128 genes was overrepresented for binding sites for the nuclear transcription factor κB. CONCLUSION: A healthy Nordic diet reduces inflammatory gene expression in SAT compared with a control diet independently of body weight change in individuals with features of the metabolic syndrome.
RCT Entities:
BACKGROUND: Previously, a healthy Nordic diet (ND) has been shown to have beneficial health effects close to those of Mediterranean diets. OBJECTIVE: The objective was to explore whether the ND has an impact on gene expression in abdominal subcutaneous adipose tissue (SAT) and whether changes in gene expression are associated with clinical and biochemical effects. DESIGN: Obese adults with features of the metabolic syndrome underwent an 18- to 24-wk randomized intervention study comparing the ND with the control diet (CD) (the SYSDIET study, carried out within Nordic Centre of Excellence of the Systems Biology in Controlled Dietary Interventions and Cohort Studies). The present study included participants from 3 Nordic SYSDIET centers [Kuopio (n = 20), Lund (n = 18), and Oulu (n = 18)] with a maximum weight change of ±4 kg, highly sensitive C-reactive protein concentration <10 mg/L at the beginning and the end of the intervention, and baseline body mass index (in kg/m²) <38. SAT biopsy specimens were obtained before and after the intervention and subjected to global transcriptome analysis with Gene 1.1 ST Arrays (Affymetrix). RESULTS: Altogether, 128 genes were differentially expressed in SAT between the ND and CD (nominal P < 0.01; false discovery rate, 25%). These genes were overrepresented in pathways related to immune response (adjusted P = 0.0076), resulting mainly from slightly decreased expression in the ND and increased expression in the CD. Immune-related pathways included leukocyte trafficking and macrophage recruitment (e.g., interferon regulatory factor 1, CD97), adaptive immune response (interleukin32, interleukin 6 receptor), and reactive oxygen species (neutrophil cytosolic factor 1). Interestingly, the regulatory region of the 128 genes was overrepresented for binding sites for the nuclear transcription factor κB. CONCLUSION: A healthy Nordic diet reduces inflammatory gene expression in SAT compared with a control diet independently of body weight change in individuals with features of the metabolic syndrome.
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