Masaru Yoshida

Obesity, along with hypertension and hyperlipidemia, is one of the leading factors of metabolic syndrome, which increases the risk of diabetes. However, controlling obesity is a global challenge. Sake lees, or Japanese rice wine lees, is a by-product of sake fermentation and has been consumed in Japan for a long time. Sake lees contains an abundance of amino acids, peptides, dietary fiber, and micronutrients, which make it highly nutritional. Additionally, sake lees has been reported to have multiple interesting effects when ingested and may aid in combating obesity. In this study, we investigated the effects of sake lees materials on preadipocyte differentiation and fat accumulation in preadipocyte cells (3T3-L1) and analyzed it with a metabolome analysis. We found that compared to the control group, lipid accumulation was suppressed by 80.9% when the 100 C-? extract of indigestible sake lees component (ISLCs) was added to 1 mg/mL. Additionally, the metabolome analysis revealed various other differences between the control group and the group treated with ISLCs, especially in amino acids concentrations. Based on the above findings, we demonstrate that ISLCs affect the amino acid metabolic pathways, which in turn affect differentiation and lipid accumulation in adipocytes. Therefore, we suggest that sake lees may aid in combating obesity and addressing metabolic syndromes, both of which can be considered as global issues. The limitation of this research is sake lee is a general non-direct edible raw material and it is difficult to add as a regular diet.

In mass spectrometry-based metabolomics, the differences in the analytical results from different laboratories/machines are an issue to be considered because various types of machines are used in each laboratory. Moreover, the analytical methods are unique to each laboratory. It is important to understand the reality of inter-laboratory differences in metabolomics. Therefore, we have evaluated whether the differences in analytical methods, with the exception sample pretreatment and including metabolite extraction, are involved in the inter-laboratory differences or not. In this study, nine facilities are evaluated for inter-laboratory comparisons of metabolomic analysis. Identical dried samples prepared from human and mouse plasma are distributed to each laboratory, and the metabolites are measured without the pretreatment that is unique to each laboratory. In these measurements, hydrophilic and hydrophobic metabolites are analyzed using 11 and 7 analytical methods, respectively. The metabolomic data acquired at each laboratory are integrated, and the differences in the metabolomic data from the laboratories are evaluated. No substantial difference in the relative quantitative data (human/mouse) for a little less than 50% of the detected metabolites is observed, and the hydrophilic metabolites have fewer differences between the laboratories compared with hydrophobic metabolites. From evaluating selected quantitatively guaranteed metabolites, the proportion of metabolites without the inter-laboratory differences is observed to be slightly high. It is difficult to resolve the inter-laboratory differences in metabolomics because all laboratories cannot prepare the same analytical environments. However, the results from this study indicate that the inter-laboratory differences in metabolomic data are due to measurement and data analysis rather than sample preparation, which will facilitate the understanding of the problems in metabolomics studies involving multiple laboratories.

Helicobacter suis, a zoonotic infection-related bacterium, can induce gastric mucosa-associated lymphoid tissue (MALT) lymphoma in humans and animals. Recently, we reported that the formation of gastric MALT lymphoma after H. suis infection is induced by interferon (IFN)-γ activation. Here, we revealed that activation of the Toll-like receptor (TLR) 4-Toll/IL-1 receptor domain-containing adapter-inducing interferon-β (TRIF) pathway after H. suis infection is associated with the production of type 1 IFNs (IFN-α, IFN-β) by gastric epithelial cells. Additionally, these type 1 IFNs interact with type 1 IFN receptors on gastric B cells, facilitating the secretion of IFN-γ and the activation of which is enhanced by positive feedback regulation in B cells. These results suggest that the TLR4-TRIF-type 1 IFN-IFN-γ pathway is crucial in the development of gastric MALT lymphoma after H. suis infection and may, therefore, represent a therapeutic target for the prevention of this condition.