Peanut sprouts (PS), which are germinated peanut seeds, have recently been reported to have anti-oxidant, anti-inflammatory, and anti-obesity effects. However, the underlying mechanisms by which PS modulates lipid metabolism are largely unknown. To address this question, serial doses of PS extract (PSE) were added to 3T3-L1 cells during adipocyte differentiation. PSE (25 µg/mL) significantly attenuated adipogenesis by inhibiting lipid accumulation in addition to reducing the level of adipogenic protein and gene expression with the activation of AMP-activated protein kinase (AMPK). Other adipocyte cell models such as mouse embryonic fibroblasts C3H10T1/2 and primary adipocytes also confirmed the anti-adipogenic properties of PSE. Next, we investigated whether PSE attenuated lipid accumulation in mature adipocytes. We found that PSE significantly suppressed lipogenic gene expression, while fatty acid (FA) oxidation genes were upregulated. Augmentation of FA oxidation by PSE in mature 3T3-L1 adipocytes was confirmed via a radiolabeled-FA oxidation rate experiment by measuring the conversion of [3H]-oleic acid (OA) to [3H]-H2O. Furthermore, PSE enhanced the mitochondrial oxygen consumption rate (OCR), especially maximal respiration, and beige adipocyte formation in adipocytes. In summary, PSE was effective in reducing lipid accumulation in 3T3-L1 adipocytes through mitochondrial fatty acid oxidation involved in AMPK and mitochondrial activation.

High fat diet-induced obesity and lipopolysaccharide-induced inflammation/inhibition of the browning of adipocytes were reversed by p-coumaric acid-enriched peanut sprouts.

Wild ginseng, Panax ginseng Meyer, is a traditional medicine widely used in Asia. Due to low reward and high costs, wild ginseng is produced by a plant cell culture technique called cultured ginseng roots (GR). The health benefits of wild ginseng have been well studied, but the potential health effects of GR are largely unknown. Thus, we investigated the role of a GR extract (GRE) on inflammatory responses. We firstly investigated the anti-inflammatory potential of GRE in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. GRE (100 μg/mL) dampened pro-inflammatory gene expression, cytokine release, reactive oxygen species (ROS) production, and mitogen-activated protein kinase (MAPK) activation. These anti-inflammatory responses by GRE were confirmed in mouse bone marrow-derived macrophages (BMDMs), which showed that GRE could inhibit inflammation with the induction of antioxidant levels. LPS was recently reported to impair mitochondrial bioenergetics in mouse macrophages. We next measured the mitochondrial oxygen consumption rate (OCR), determining mitochondrial function. LPS treatment downregulated OCR; however, GRE partially restored the LPS-mediated energy homeostasis defects. Furthermore, GRE-pretreated conditioned media (CM) obtained from mouse macrophages decreased CM-mediated adipocyte inflammation. Collectively, these data suggested that GRE attenuated LPS-induced inflammation, and it might be partially involved in the protection from mitochondrial dysfunction in macrophages and adipocytes.

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).