Showing papers by "Chang Hwa Jung published in 2019"

Fermentation Improves the Preventive Effect of Soybean Against Bone Loss in Senescence-Accelerated Mouse Prone 6.

Abstract: Osteopenia is a preclinical phase of osteoporosis, it occurs naturally with aging and increases the risk of bone fractures in elderly males. Previous studies have revealed the beneficial effects of soybean on preventing bone loss due to its isoflavone contents. Fermentation alters the soybean isoflavone contents, that is, isoflavone glucosides is hydrolyzed into aglycones. However, it is not clear how these alterations influences the preventive effect of soybean on bone loss. In this study, we fed senescence-accelerated mouse prone 6 (SAMP6), a model of senile osteopenia, with an equal dosage of nonfermented soybean (NS) or fermented soybean, Doenjang (DJ) for 18 weeks. Mice supplemented with DJ showed 1.13-fold higher bone densities and 1.06-fold longer relative bone lengths than those of osteopenic SAMP6 mice old control (OC), while NS-supplemented mice showed no significant improvement. Supplementation with DJ effectively prevented bone loss in the osteopenia model by the improvement of bone formation and reduction of osteoclastogenesis. In addition, we discovered that DJ increased osteogenesis in SAMP6 mice via BMP2-Smad-Runx2 signaling. These results suggest that the fermentation process could enhance bone loss prevention by soybean and dietary supplementation with fermented soybeans may be beneficial for bone health. PRACTICAL APPLICATION: Soybean fermentation improved the preventive effects of soybean on bone loss. Therefore, the consumption of fermented soybean, Doenjang, is a potential alternative for aging-related bone loss therapy.

Lotus Leaf Ethanol Extract and Nuciferine Suppress Adipocyte Differentiation by Regulating Akt-mTORC1 Signaling in 3T3-L1 Cells

Abstract: Lotus leaf has been reported to exert anti-inflammatory, hypolipidemic, and hepatoprotective effects. However, the effect of lotus leaf on adipocyte differentiation and its action mechanism have not been clarified. In this study, 3T3-L1 preadipocytes were incubated with or without lotus leaf ethanol extract (EEN) for 8 days. Microscopic inspection and Oil Red O staining indicated that EEN treatment significantly reduced adipogenesis in 3T3-L1 cells. EEN also downregulated the protein levels of adipogenic transcription factors including sterol regulatory element binding protein 1 (SREBP1), peroxisome proliferator-activated receptor-gamma (PPARγ), and CCAAT/enhancer binding protein α (C/EBPα), and target genes such as adipocyte binding protein 2 (aP2) and fatty acid synthase (FAS) in a dose-dependent manner. In order to understand whether nuciferine, the primary active component of EEN contributed to the anti-adipogenic activity of EEN, we examined the effect of nuciferine on adipogenesis related gene expression. Nuciferine significantly reduced expression of adipogenic transcription factors and target genes. Notably, nuciferine downregulated the phosphorylation of Akt, mammalian target of rapamycin complex 1 (mTORC1), S6K, and 4EBP1. These results suggest that lotus leaf ethanol extract exerts anti-adipogenic activity, and could be partially mediated through the regulation of the Akt-mTORC1 signaling pathway by nuciferine.

Pear Extract and Malaxinic Acid Reverse Obesity, Adipose Tissue Inflammation, and Hepatosteatosis in Mice.

Abstract: Scope Obesity and diabetes are major public health problems and are emerging as pandemics. Considerable evidence suggests that pear fruit consumption is associated with a lower risk of obesity-related complications. Thus, the present study is conducted to investigate the therapeutic potential of pear extract (PE) for reversing obesity and associated metabolic complications in high-fat diet-induced obese mice. Methods and results Obesity is induced in male C57BL/6 mice fed a high-fat diet for 11 weeks. After the first 6 weeks on the diet, obese mice are administered vehicle or PE for 5 weeks. PE treatment decreases body weight gain, expands white adipose tissue (WAT), and causes hepatic steatosis in obese mice, as well as inhibits adipogenesis and lipogenesis. Impaired glucose tolerance and insulin resistance are improved by PE. In addition, PE reduces macrophage infiltration and expression of pro-inflammatory genes and deactivates mitogen-activated protein kinases in WAT. Finally, malaxinic acid is identified as an active component responsible for the anti-obesity effects of PE in mice. Conclusion The results demonstrate that PE supplementation ameliorates diet-induced obesity and associated metabolic complications and suggest the health-beneficial effects of both pear fruits and malaxinic acid in counteracting these diseases.