P-Coumaric Acid Enriched-Peanut Sprout Improves High Fat Diet-Induced Obesity and Insulin Resistance by Inhibiting Macrophage Recruitment

Abstract

Abstract Objectives We have previously reported that Peanut Sprout Extract (PSE) inhibited adipogenesis through augmentation of mitochondrial fatty acid oxidation. However, it is unknown whether PS consumption reduced visceral obesity and obesity-mediated metabolic complications in vivo. Methods To test this question, obesity-prone C57BL/6 male mice were randomly assigned into three different group; 1) low-fat (LF) diets (11% calories from fat), 2) high-fat (HF) diets (60% calories from fat) or 2) HF diets plus PS (4% in diet, HF-P). Results HF diet for 8 weeks resulted in a significant increase in body weight, liver, and adipose tissue mass compared to LF alone. PS supplementation reduced 1) body weight gain, 2) lipid profile, 3) up-regulated glucose levels, and 4) recruitment of adipose tissue macrophage in HF diet-induced obese C57BL6 mice. In parallel, lipopolysaccharide (LPS)-mediated induction of inflammation was reversed by PSE treatment in macrophages and adipocytes with significant suppression of MAP kinase and NF-kB activation. PSE also reduced LPS-mediated M1 macrophage polarization in bone marrow stem cells. Additionally, we found that, among constitutes of PSE, p-coumaric acid has been identified as responsible polyphenol that exclusively showed a similar trends as PSE. Conclusions Collectively, these data suggest that p-coumaric acid enriched-Peanut Sprout attenuates visceral obesity and obesity-mediated metabolic complications by inhibiting adipose inflammation. Funding Sources This work has supported by the National Research Foundation of Korea(NRF) grant funded by the Korea government (MSIT).