The University of Osaka · Medicine
Professor Yuya Fujishima's research lab focuses on the pathophysiological roles of adipokines, particularly adiponectin and its receptor T-cadherin, in metabolic and vascular diseases. The lab investigates how adiponectin signaling through T-cadherin influences atherosclerosis, kidney injury, and insulin resistance, with a strong emphasis on vascular and renal cell biology. Additional research explores the roles of enzymes such as xanthine oxidoreductase and glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) in metabolic syndrome, nonalcoholic fatty liver disease (NAFLD), and systemic inflammation. The lab integrates preclinical models with clinical observations to uncover novel mechanisms linking adipose tissue-derived factors to organ protection and disease progression.
Figures are computed from collected data and may differ slightly.
Adiponectin, an adipocyte-derived protein abundant in the circulation, is thought to be protective against atherosclerosis. However, it is not fully understood how the association of adiponectin with vascular cells and its antiatherogenic effect are connected. In this study, T-cadherin was essential for accumulation of adiponectin in the neointima and atherosclerotic plaque lesions, and the adiponectin-T-cadherin association protected against vascular injury. In the apolipoprotein E-knockout (Ap
Serum selenium levels were inversely associated with death risk, especially death risk due to infectious disease, among hemodialysis patients. Decreased serum selenium level may contribute to immunity dysfunction and may increase the risk of death from infectious disease in hemodialysis patients.
Liraglutide produced meaningful long-term weight loss and significantly improved eating behavior in obese Japanese patients with type 2 diabetes.
Adiponectin (APN) is a circulating protein specifically produced by adipocytes. Native APN specifically binds to T-cadherin, a glycosylphosphatidylinositol-anchored protein, mediating the exosome-stimulating effects of APN in endothelial, muscle, and mesenchymal stem cells. It was previously reported that APN has beneficial effects on kidney diseases, but the role of T-cadherin has not been clarified yet. Here, our immunofluorescence study indicated the existence of both T-cadherin and APN prote
Xanthine oxidoreductase (XOR) is an enzyme that catalyzes hypoxanthine to xanthine and xanthine to uric acid, respectively. However, the underlying mechanisms of increased plasma XOR and its pathological roles in systemic diseases, such as atherosclerosis, are not fully understood. In this study, we found that changes in plasma XOR activity after bariatric surgery closely associated with those in liver enzymes, but not with those in BMI. In a mouse model of nonalcoholic fatty liver disease/steat
Glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) is an enzyme that specifically cleaves GPI anchors. Previous human studies suggested the relationship of GPI-PLD to insulin resistance, type 1 and type 2 diabetes, and nonalcoholic fatty liver disease (NAFLD). However, the biological roles of GPI-PLD have not been elucidated. Here, we hypothesized that GPI-PLD impacted on lipid and glucose metabolism, especially in the liver. GPI-PLD mRNA was most highly expressed in the liver, and
Visceral fat-based metabolic syndrome has a strong impact on atherosclerotic cardiovascular disease (CVD), clustering diabetes, dyslipidemia, hypertension, hyperuricemia, and non-alcoholic fatty liver disease (NAFLD). Adiponectin, a protein specifically secreted by adipocytes, circulates abundantly in the human bloodstream, but its concentration decreases under pathological conditions such as visceral fat accumulation. Extensive clinical evidence has demonstrated that hypoadiponectinemia is asso
Topiroxostat improved arterial stiffness parameters in hyperuricemic patients with liver dysfunction, which might be related to its inhibitory effect on plasma XOR.
Our findings from this pilot study demonstrated that abdominal-obese individuals had greater preferences for fat and carbohydrates, which were linked to actual fat and carbohydrate intake and possibly contributed to the development of obesity.
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