Naringenin suppresses macrophage infiltration into adipose tissue in an early phase of high-fat diet-induced obesity

H Yoshida, H Watanabe, A Ishida, W Watanabe… - Biochemical and …, 2014 - Elsevier
H Yoshida, H Watanabe, A Ishida, W Watanabe, K Narumi, T Atsumi, C Sugita, M Kurokawa
Biochemical and biophysical research communications, 2014Elsevier
Obese adipose tissue is characterized by increased macrophage infiltration, which results in
chronic inflammation in adipose tissue and leads to obesity-related diseases such as type 2
diabetes mellitus and atherosclerosis. The regulation of macrophage infiltration into adipose
tissue is an important strategy for preventing and treating obesity-related diseases. In this
study, we report that naringenin, a citrus flavonoid, suppressed macrophage infiltration into
adipose tissue induced by short-term (14 days) feeding of a high-fat diet in mice; although …
Abstract
Obese adipose tissue is characterized by increased macrophage infiltration, which results in chronic inflammation in adipose tissue and leads to obesity-related diseases such as type 2 diabetes mellitus and atherosclerosis. The regulation of macrophage infiltration into adipose tissue is an important strategy for preventing and treating obesity-related diseases. In this study, we report that naringenin, a citrus flavonoid, suppressed macrophage infiltration into adipose tissue induced by short-term (14 days) feeding of a high-fat diet in mice; although naringenin did not show any differences in high-fat diet-induced changes of serum biochemical parameters in this short administration period. Naringenin suppressed monocyte chemoattractant protein-1 (MCP-1) in adipose tissue, and this effect was mediated in part through inhibition of c-Jun NH2-terminal kinase pathway. Naringenin also inhibited MCP-1 expression in adipocytes, macrophages, and a co-culture of adipocytes and macrophages. Our results suggest a mechanism by which daily consumption of naringenin may exhibit preventive effects on obesity-related diseases.
Elsevier