The hypertrophic adipocytes of
obese subjects are overloaded with stored triacylglycerol and
it is likely that the buffering capacity for further lipid storage
in these adipocytes is decreased, especially in the postprandial
state. Non-adipose tissues are therefore exposed to an excessive
influx of lipids which could lead to ectopic fat deposition
[31]. Adipose tissue is often considered to be an abundant
source of pro-inflammatory mediators [32]. Systemic inflammation
is considered a hallmark of COPD [33] and increased
levels of pro-inflammatory mediators have been reported in
the circulation of COPD patients [30].