Diet and exercise reduce low-grade inflammation and macrophage infiltration in adipose tissue but not in skeletal muscle in severely obese subjects.
Obesity is associated with low-grade inflammation, insulin resistance, type 2 diabetes, and cardiovascular disease. This study investigated the effect of a 15-wk lifestyle intervention (hypocaloric diet and daily exercise) on inflammatory markers in plasma, adipose tissue (AT), and skeletal muscle (SM) in 27 severely obese subjects (mean body mass index: 45.8 kg/m2). Plasma samples, subcutaneous abdominal AT biopsies, and vastus lateralis SM biopsies were obtained before and after the intervention and analyzed by ELISA and RT-PCR. The intervention reduced body weight (P < 0.001) and increased insulin sensitivity (homeostasis model assessment; P < 0.05). Plasma adiponectin (P < 0.001) increased, and C-reactive protein (P < 0.05), IL-6 (P < 0.01), IL-8 (P < 0.05), and monocyte chemoattractant protein-1 (P < 0.01) decreased. AT inflammation was reduced, determined from an increased mRNA expression of adiponectin (P < 0.001) and a decreased expression of macrophage-specific markers (CD14, CD68), IL-6, IL-8, and tumor necrosis factor-alpha (P < 0.01). After adjusting for macrophage infiltration in AT, only IL-6 mRNA was decreased (P < 0.05). Only very low levels of inflammatory markers were found in SM. The intervention had no effect on adiponectin receptor 1 and 2 mRNA in AT or SM. Thus hypocaloric diet and increased physical activity improved insulin sensitivity and reduced low-grade inflammation. Markers of inflammation were particularly reduced in AT, whereas SM does not contribute to this attenuation of whole body inflammation.
Bruun
Jens M
JM
Dept. of Endocrinology and Metabolism, Aarhus University Hospital, Aarhus Sygehus, Tage Hansensgade 2, DK-8000 Aarhus C, Denmark. Jens.Bruun@ki.au.dk
Helge
Jørn W
JW
Richelsen
Bjørn
B
Stallknecht
Bente
B
D052242:Adiponectin / Q000097:blood / Q000235:genetics; D000273:Adipose Tissue / Q000473:pathology*; D015703:Antigens, CD / Q000235:genetics; D015214:Antigens, Differentiation, Myelomonocytic / Q000235:genetics; D001794:Blood Pressure / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D002097:C-Reactive Protein / Q000032:analysis; D018932:Chemokine CCL2 / Q000097:blood / Q000235:genetics; D004032:Diet; D015444:Exercise / Q000502:physiology*; D005260:Female; D015870:Gene Expression / Q000235:genetics; D005951:Glucose Tolerance Test; D006801:Humans; D007249:Inflammation / Q000473:pathology; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D016209:Interleukin-8 / Q000097:blood / Q000235:genetics; D018950:Lipopolysaccharide Receptors / Q000235:genetics; D008264:Macrophages / Q000473:pathology; D008297:Male; D018482:Muscle, Skeletal / Q000473:pathology*; D009765:Obesity / Q000473:pathology* / Q000628:therapy; D054419:Receptors, Adiponectin; D011956:Receptors, Cell Surface / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000235:genetics; D000097382:CD68 Molecule
D052242:Adiponectin; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D002097:C-Reactive Protein; D018932:Chemokine CCL2; D015850:Interleukin-6; D016209:Interleukin-8; D018950:Lipopolysaccharide Receptors; D054419:Receptors, Adiponectin; D011956:Receptors, Cell Surface; D014409:Tumor Necrosis Factor-alpha; C475418:ADIPOR1 protein, human; C475420:ADIPOR2 protein, human; C111835:CCL2 protein, human; C067980:CD68 antigen, human; D000097382:CD68 Molecule