Adipositas & Bewegung

Abstract

The prevalence of obesity is continuously risingworldwide. Obesity is the result of a lasting metabolic surplus which leads to pathological expansion of adipose tissue (AT). Beside a subset of apparently metabolically-healthy obese individuals, the majority of obese subjects develop an increased risk for type 2 diabetes mellitus (T2D), coronary heart disease (CHD), and several other "western world"diseases. In these individuals,AT expansion is associated with metabolic stress responses in adipocytes followed by the induction of signals ofinnate immune response. Downstream, these processes are followed by translocation of NfB into the nucleus, leading to the expression of various inflammatory cytokines and chemokines in AT. Infiltrating leukocytes amplify inflammation leading to a "spill-over"to the blood stream. Beside the negative effects of inflammatory mediators on endothelial function, inflammation is transferred to various other organs and tissues like liver, muscle, gut, and brain. Regular physical activity increases energy turnover followed by a decrease of visceral fat mass. Subsequently, metabolic stress and its inflammatory consequences are reduced. Beside the metabolic effects,exercise also directly affects humoral and cellular immune activation. Inflammatory processes in AT are diminished followed by a reduced spill-over of inflammation to the blood stream. Exercise training is also effective in reducing pathophysiological consequences of obesity locally in tissues like muscle, gut, and brain.KEY WORDS: Adipose Tissues, Cytokines, Leukocytes, Physical Activity, Immune System, Adipocytes