Fat depot-specific differences of macrophage infiltration and cellular senescence in obese bovine adipose tissues.

Abstract

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.