Obesity is associated with the chronic inflammation and senescence of adipose tissues.
Macrophage is a key mediator of chronic inflammation that infiltrates obese adipose tissue
and stimulates metabolic disorders. However, the fat depot-specific differences of
macrophage infiltration and senescence, especially the influence on intramuscular adipose
tissue, have remained unclear. We investigated the fat depot-specific differences of
macrophage infiltration and senescence in obese bovine adipose tissue from three different
anatomical sites (subcutaneous, intramuscular and visceral). Macrophage infiltrations and
crown-like structures were observed in visceral adipose tissue, although there were few
macrophages in subcutaneous and intramuscular adipose tissues. The positive reaction of
senescence marker SA-βgal activity was observed in visceral adipose tissue. In contrast,
the activity of SA-βgal in subcutaneous and intramuscular adipose tissues were low. The
expression of p53 gene, the master regulator of cellular senescence, in visceral adipose
tissue was higher than that of subcutaneous and intramuscular adipose tissue. At the
cellular level, p53 gene expression was negatively correlated with the size of
subcutaneous adipocytes. In contrast, p53 gene expressions were positively correlated with
the size of intramuscular and visceral adipocytes. These results indicate that anatomical
sites of obese adipose tissue affect macrophage infiltration and the senescent state in a
fat depot-specific manner.