Lysophosphatidic acid (LPA) and sphingosylphosphorylcholine (SPC) activated Fyn tyrosine kinase and induced stress fiber formation, which was blocked by pharmacological inhibition of Fyn, gene silencing of Fyn, or dominant negative Fyn. Overexpressed constitutively active Fyn localized at both ends of F-actin bundles and triggered stress fiber formation, only the latter of which was abolished by Rho-kinase (ROCK) inhibition. SPC, but not LPA, induced filopodia-like protrusion formation, which was not mediated by Fyn and ROCK. Thus, Fyn appears to act downstream of LPA and SPC to specifically stimulate stress fiber formation mediated by ROCK in fibroblasts.
Summary Group B soyasaponins, found in soy, have various health-promoting properties, but it is unclear whether they have an anti-obesity effect. The aim of this study was to evaluate the anti-obesity effect of group B soyasaponin glycosides and aglycone in mice fed a high-fat diet. Six-week-old C57/BL6 mice were divided into three groups (each n510) and orally administered a high-fat diet for 35 d; two of the groups also received group B soyasaponin glycosides or aglycone. Although there was no significant difference among the three groups in consumption, the weight of fat adipose tissue at autopsy was more than 30% lower in the group B soyasaponin aglycone group than in the control group, but X-ray computed tomography showed no significant difference in muscle weight between these two groups. The ratio of muscle to whole body weight was higher in the group B soyasaponin aglycone group than in the control group. These results suggest that group B soyasaponin aglycone has a stronger anti-obesity effect than group B soyasaponin glycosides, without a loss in muscle weight, and that it increases the ratio of muscle to whole body weight. To our knowledge, this is the first report showing the anti-obesity effect of soyasaponin aglycone in vivo using animal models.
Soyasapogenol is a soyasaponin aglycone, which has been suggested to exert a more potent function than the glycoside form. In this study, the effect of soyasapogenol A and B on cultured adipocyte cell function was investigated using mouse 3T3-L1 adipocyte cells. 3T3-L1 cells were treated with insulin, dexamethasone, and 3-isobutyl-1-methylxanthine for differentiation to adipocytes, and the cells were then cultured in the presence of soyasapogenol A or B (6.25 or 12.5 µM). The media were harvested and refreshed every 2 d. After a 10 d culture, the cells were harvested and the triglyceride content of the cells was determined. The triglyceride content of soyasapogenol B-treated cells was significantly lower than those of vehicle-treated cells. Glycerol and free fatty acid levels in the soyasapogenol-treated cell media were higher than those in vehicle cells. However, there was no difference in the level of adipose triglyceride lipase among soyasapogenol A-, soyasapogenol B-, and vehicle-treated cells. The secreted adiponectin and resistin levels of soyasapogenol-treated cell media were also different compared with those of vehicle-treated cells. Especially, the secreted resistin level in soyasapogenol B-treated cell media was obviously reduced compared with that of vehicle-treated cells. Taken together, these results suggest that soyasapogenol B exerted an anti-obesity and anti-diabetic effect on adipocytes by lowering the cellular triglyceride level by accelerating triglyceride lipolysis with reduced resistin secretion.
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