Establishment of nutrient renal medicine -lessoned from starvation-

2016 Fiscal Year Final Research Report

• Project/Area Number: 25713033
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Kidney internal medicine
• Research Institution: Shiga University of Medical Science
• Principal Investigator: Kume Shinji 滋賀医科大学, 医学部, 助教 (00452235)
• Research Collaborator: TAKAGI Ayano ; YAMAHARA Mako ; TAGAWA Atsuko ; KUWAGATA Shogo ; Ono Shinya ; TANAKA Yuki
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: 腎臓 / 飢餓 / 糖尿病性腎症 / mTORC1 / オートファジー / NAD代謝

Outline of Final Research Achievements

This study revealed the novel physiological role of kidney to combat starvation. Renal autophagy is essential for hepatic and renal ketogenesis during starvation. Furthermore, we concluded that some renal nutrient-sensing signals and autophagy are associated with the pathogenesis of diabetic nephropathy. 1) Fatty acids are novel nutrient factors to regulate mTORC1 lysosomal localization and apoptosis in podocytes. 2) MicroRNA148b-3p inhibits mTORC1-dependent apoptosis in diabetes by repressing TNFR2 in proximal tubular cells. 3) Impaired podocyte- and proximal tubular cell-autophagy exacerbate proteinuria-related kidney injury in diabetic nephropathy. 4) 1-Methylnicotinamide ameliorates lipotoxicity-induced oxidative stress and cell death in kidney proximal tubular cells. 5) O-linked β-N-acetylglucosamine modification of proteins is essential for foot process maturation and survival in podocytes.

Free Research Field

腎臓内科