Improvement in High-fat Diet-induced Obesity and Insulin Resistance upon Uptake of PS-B1, a Fermented Product Prepared from Soy Flour Using Lactic Acid Bacteria

PS-B1 is a fermented product prepared from soy flour using lactic acid bacteria. Over a 10-week period, C57BL/6J mice were reared under laboratory conditions on a normal diet (control, n=5), high-fat diet (HF, n=5), or high-fat diet supplemented with 4% PS-B1 (HF-P, n=6). After 10 weeks, the change in weight gain, intestinal and epididymal fat accumulation, serum and liver biochemical parameters, and gene expression in the mice was investigated. HF diet-induced weight gain and increase in intestinal and epididymal fat accumulation were lower in mice fed with HF-P diet than in mice fed with HF diet, suggesting that PS-B1 prevented HF diet-induced obesity in HF-P mice. Furthermore, the levels of liver lipids (triglycerides, TG; non-esterified fatty acid, NEFA; total cholesterol, TC), serum TC, serum glucose, and serum insulin were significantly increased in the HF group than those in control mice. In HF-P mice, neither serum TC nor serum glucose levels were reduced. In contrast, the levels of liver lipids and serum insulin were lower in HF-P mice than in HF mice, suggesting that PS-B1 reduced these parameters in HF-P mice. The homeostatic model assessment of insulin resistance (HOMA-IR) value, which was calculated from the serum glucose and insulin levels, was 21.5 ± 4.2 in the HF mice. However, the HOMA-IR (8.2 ± 0.2) values were significantly decreased in the HF-P mice, suggesting that PS-B1 improves insulin resistance. Additionally, we compared the expression levels of stearoyl-CoA desaturase-1 (Scd1) in the liver. Quantitative RT-PCR showed increased expression of Scd1 in HF mice compared to that in control mice. Furthermore, ingestion of PS-B1 led to reduced expression of Scd1 mRNA in HF-P mice, implying that PS-B1 is effective in reducing the expression of the gene encoding SCD1. These results suggest that the anti-obesity effect of PS-B1 and improvement in fat accumulation upon PS-B1 uptake may be due to improvement in insulin resistance and reduction in the expression level of Scd1.