[Obesity as inflammatory disease].
Studies of the role of immune system activation in the pathogenesis of obesity and its concomitant diseases have been conducted for some years. Numerous recent studies revealed an association between increased immune activation in obesity and the development of insulin resistance. On the other hand there is the hypothesis that immune activation in obesity is a homeostatic mechanism to protect the organism from reaching the point at which the over-accumulation of fat decreases the possibility to move. The aim of the present study was to review the current literature on immune activation in obesity and the participation of adipokines produced by adipose tissue in the development of insulin resistance. Attention is drawn to the similarities in function and gene expression of adipocytes and macrophages.
Olszanecka-Glinianowicz
Magdalena
M
Katedra Patofi zjologii Slaskiego Uniwersytetu Medycznego w Katowicach. magols@esculap.pl
Zahorska-Markiewicz
Barbara
B
D017667:Adipocytes / Q000378:metabolism; D054392:Adipokines / Q000096:biosynthesis*; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D015870:Gene Expression; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D007333:Insulin Resistance / Q000276:immunology; D015850:Interleukin-6 / Q000378:metabolism; D020738:Leptin / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D009765:Obesity / Q000276:immunology* / Q000378:metabolism; D052243:Resistin / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D054392:Adipokines; D015850:Interleukin-6; D020738:Leptin; D052243:Resistin; D014409:Tumor Necrosis Factor-alpha