Japan’s Kanazawa University launches Institute for Frontier Science Initiative（InFiniti）its flagship multi-million dollar global research-hub in interdisciplinary research in core areas including controlling cancer progression; innovative integrated bioscience; and creating future societies.
Kanazawa University is one of Japan’s premier education and research institutes with three colleges and 16 schools offering courses in subjects that include medicine, computer engineering, and humanities.
The Institute for Frontier Science Initiative（InFiniti）is Kanazawa University’s new multi-million dollar flagship interdisciplinary research hub where international groups of scientists will undertake research in areas including diagnosis and treatment of ‘nutrition related’ diseases such as diabetes and cancer; archaeology and cultural resource management; and so-called ‘supramolecules’ and ‘proton-conducting’ solids for next-generation fuel cells. Notably, research at Infiniti will be conducted by approximately 1000 scientists, covering 85 topics with annual research funding of approximately US$4 million.
“We welcome scientists from all over the world to collaborate with us in the search for long term solutions to global issues in medicine, energy, management of the world’s cultural heritage, and a sustainable society,” says Shinichi Nakamura, the Director of InFiniti. “Scientists can join us at Kanazawa in Japan or collaborate based at their own institutes.”
The Institute for Frontier Science Initiative also has funding for establishing joint degrees programs, student exchange, and hiring of ‘university research administrators’ to promote and support the project on a global scale.
Research highlight by scientists at InFiniti
Journal: Cell Reports 14, pp.1–13, March 15, 2016.
Institute for Frontier Science Initiative research: Mechanism revealed linking liver disease and obesity
Researchers find similarities in the impeded signalling between central insulin activity and glucose production in the liver for both obese mice and mice that have had the vagus nerve removed.
The vital role of insulin in controlling glucose production is often disrupted in people suffering from obesity, a condition approaching global epidemic levels. Previous work has shown that central insulin action suppresses glucose production in the liver by increasing levels of the ligand interleukin 6 (IL-6) in the liver. The ligand activates the transcription factor STAT3, which in turn suppresses gene expression of glucose-producing enzymes. However, how the liver communicates with central nervous system and the vagus nerve, which controls unconscious processes like digestion, has so far not been understood.
Now a collaboration of researchers in Japan led by Hiroshi Inoue at Kanazawa University’s Institute for Frontier Science Initiative (InFiniti) has identified the molecular mechanism for this communication.
The researchers investigated the effects of administering chlorisondamine, which prevents α7-nicotinic acetylcholine receptor activity, as well as removal of the vagal nerve. They found that while STAT3 phosphorylation and IL-6 expression in the liver increased only slightly the IL-6/STAT3 signalling response to administered insulin was lost.
The researchers compared the response in regular and obese mice and found that the administered insulin “failed to elicit changes in vagus nerve activity of high-fat diet-induced obese mice.” They conclude, “These findings suggest that the aberrant regulation of Kupffer cells via the vagus nerve and α7-nAchR-mediated cholinergic action by central insulin action may have a significant role in the pathogenesis of chronic hepatic inflammation in obesity.”