Basic Medicine, Physiology, Genomics, Genetics and Epigenetics

Molecular Physiology and Metabolism

We Elucidate Epigenome, Chemical Modifications on Genome that Confer “Cellular Memory” and Suggested to Be Involved in “Predisposition” to Life Style Diseases. We Develop Tools for Dynamical Analysis of Protein-protein Interaction

Medical Sciences Course

  • Master / Doctoral Degree



Professor, M.D., Ph.D

Research Theme

  • Epigenome and Metabolic syndrome
  • Adipogenesis and obesity
  • Lipid Metabolism
Research Keywords:

Metabolic syndrome, Adipocyte and obesity, Epigenome, Cholesterol, Metabolism

Technical Keywords:

Adipogenesis, Proteomics, ChIP sequencing, Epigenome analysis, Gene knock-out/knock-in mouse

Laboratory Introduction

Epigenetics, from the Greek "epi," means "on," DNA. All of our tissues contain the same 33,000 genes; however, in a given tissue and at a given stage, owing to an "epigenetic code," only a few of these genes are expressed, giving rise to the "phenotype". Disruption of the balance of epigenetic networks may cause several major diseases, including cancer, syndromes involving chromosomal instabilities, and mental retardation. However, the relevance of epigenetics to other physio-pathological mechanisms in common diseases, such as metabolic syndrome, was less clear. Our laboratory is now focusing on solving the physio-pathological mechanisms in metabolic syndrome by studying the epigenetic network.
Especially, we are focusing on metabolic syndrome and fat cells (adipocytes). At the molecular levels, we are focusing nuclear proteins (nuclear receptor and histone modification enzymes) regulating human disease. We express target proteins and make crystals to determine super fine structure. Using this information, we are developing tools for dynamical analysis of protein-protein interaction or protein-low molecular weight compounds interaction. Our current research focuses on studying the link between energy imbalance and incorrect "epigenetic programming" in the development of obesity because of inadequate maternal nutrition and/or metabolic disturbances.

Figure 1. Obesity and metabolic syndrome in histone demethylase JMJD1A deficient mice

Figure 1. Obesity and metabolic syndrome in histone demethylase JMJD1A deficient mice

Figure 2. Elucidation of Mechanism by Integrated Epigenome Analysis

Figure 2. Elucidation of Mechanism by Integrated Epigenome Analysis

Recent Publications

  • Abe Y, Fujiwara Y, Takahashi H, Matsumura Y, Sawada T, Jiang S, Nakaki R, Uchida A, Nagao N, Naito M, Kajimura S, Kimura H, Osborne TF, Aburatani H, Kodama T, Inagaki T, Sakai J.(2018) Histone demethylase JMJD1A coordinates acute and chronic adaptation to cold stress via thermogenic phospho-switch. Nat Commun. 2018 Apr 19;9(1):1566. doi: 10.1038/s41467-018-03868-8.
  • Inagaki T, Sakai J, Kajimura S. (2016) Transcriptional and epigenetic control of brown and beige adipose cell fate and function. Nat Rev Mol Cell Biol, 17, 480-95.
  • Matsumura Y, et al. (2015) H3K4/H3K9me3 Bivalent Chromatin Domains Targeted by Lineage-Specific DNA Methylation Pauses Adipocyte Differentiation. Mol Cell, 60, 584-96.
  • Abe Y, et al. (2015) JMJD1A is a signal-sensing scaffold that regulates acute chromatin dynamics via SWI/SNF association for thermogenesis. Nat Commun, 6, 7052.
  • Sakakibara I, et al. (2009) Fasting-induced hypothermia and reduced energy production in mice lacking acetyl-CoA synthetase 2. Cell Metab, 9, 191-202.