Development of a new method for improving physical ability of chronic renal failure patients by correcting mitochondrial metabolism using electron carriers

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19465
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Kidney internal medicine
• Research Institution: Keio University
• Principal Investigator: Mitsuishi Masanori 慶應義塾大学, 医学部(信濃町), 特任助教 (50468485)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 骨格筋ミトコンドリア / サルコペニア / 慢性腎不全 / 身体能力 / グレリン / アミノレブリン酸

Outline of Final Research Achievements

Ghrelin administration on 5/6 nephrectomized mice improved skeletal muscle mitochondrial function, increased skeletal muscle mass, and improved physical performance. Ghrelin administration improved mitochondrial biogenesis through epigenomic modification of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1a) and it was suggested that increasing both muscle mass and mitochondrial content by ghrelin would improve sarcopenia associated with CKD efficiently.On the other hand, amino levulinic acid (ALA) administration increased skeletal muscle mitochondrial function, muscle mass and physical function. ALA administration increased mitochondrial biogenesis. In metabolome studies, branched chain amino acids in skeletal muscle were increased by administration of ALA. It was thought that ALA increased skeletal muscle mass through the metabolic changes in skeletal muscle.

Free Research Field

内分泌代謝学