Inflammation status in adipose tissue and peritoneal macrophages of young and old mice in diet‐induced obesity

Abstract

Obesity causes a low grade inflammation. We have shown that aging is also associated with upregulated inflammation in adipose tissue. In this study, we investigated effect of diet‐induced obesity on inflammation status in young and old mice. Young (2‐mo) and old (19‐mo) C57BL/6 mice were fed low fat (10%, LF) or high fat (60%, HF) diet for 5 mo. While body weight increased in both age groups, young mice gained more than the old. Of 13 mice in each age and diet group, none of the young and 2 old mice in LF group, and 2 young and 4 old mice in HF group died before the end of study. Adipose tissue from old LF mice expressed higher levels of IL‐1β, IL‐6, TFN‐α, and cyclooxygenase‐2 mRNA compared with young LF mice. Expression of all these inflammatory markers increased in young HF mice to levels comparable to those in old LF mice while old HF mice had lower expression of these markers compared with those in old LF mice. Adipocytes from old LF mice produced more IL‐6, TNF‐α, and prostaglandin (PG)E2 than those from young LF mice. HF resulted in increase of all of these markers in young, but only PGE2 in old mice. No significant diet‐ or age‐related difference was found in these markers in stromal vascular cells. PGE2 produced by peritoneal macrophages was upregulated with aging and HF induced more production of IL‐6 and PGE2 in young but not in old mice. Thus, obesity induces an inflammatory state in both visceral fat and peritoneal macrophages in young mice. The lack of such changes or even a decrease in some of inflammatory markers in old mice may be due to deteriorated health condition and loss of weight in some old mice fed HF. Supported by USDA #58‐1950‐7‐707.