Abstract
The failure of Kupffer cells (KCs) to remove endotoxin is an important factor in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). In this study, the effects of exercise training on KC function were studied in terms of in vivo endotoxin clearance and inflammatory responses. Mice were allocated into rest and exercise groups. KC bead phagocytic capacity and plasma steroid hormone levels were determined following exercise training. Endotoxin and inflammatory cytokine levels in plasma were determined over time following endotoxin injection. KC bead phagocytic capacity was potentiated and clearance of exogenously-injected endotoxin was increased in the exercise group. Inflammatory cytokine (TNF-α and IL-6) levels were lower in the exercise group. We found that only DHEA was increased in the plasma of the exercise group. In an in vitro experiment, the addition of DHEA to RAW264.7 cells increased bead phagocytic capacity and attenuated endotoxin-induced inflammatory responses. These results suggest that exercise training modulates in vivo endotoxin clearance and inflammatory responses in association with increased DHEA production. These exercise-induced changes in KC capacity may contribute to a slowing of disease progression in NAFLD patients.
Highlights
The problem of obesity continues to worsen as a result of several factors including the westernization of dietary habits and chronic insufficient exercise
We investigated the effects of exercise training on Kupffer cells (KCs) function, on foreign-body phagocytic capacity, in vivo endotoxin clearance, and the inflammatory response to endotoxin
® mice following the 3-month period, we injected Clophosome -A (FormuMax Scientific) at 8 μL/g body weight immediately following the exercise load. We identified this group as the 3-month rest group with Clophosome-A (Lipo3moR) and the 3-month exercise group with Clophosome-A (Lipo3moTr)
Summary
The problem of obesity continues to worsen as a result of several factors including the westernization of dietary habits and chronic insufficient exercise. Endotoxaemia and the activated KC inflammatory response, both associated with the KCs dysfunction, led to chronic inflammation in the liver. This suggests that abnormalities in KC phagocytic capacity may cause a reduction in in vivo endotoxin clearance, leading to progression of inflammatory liver disease. These conditions are assumed to be involved in the aggravation of NAFLD hepatic lesions and the progression from simple steatosis to NASH. There is insufficient evidence in support of exercise therapy as an effective modality, compared with diet therapy
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