Ken-ichi Miyamoto

TL;DR: It is demonstrated that the pathways for reactive oxygen species (ROS) production and oxidative stress are coordinately up-regulated in both the liver and adipose tissue of mice fed an HFD before the onset of insulin resistance through discrete mechanism.

TL;DR: It is demonstrated that selenoprotein P (SeP), a liver-derived secretory protein, causes insulin resistance and suggested that SeP may be a therapeutic target for type 2 diabetes.

TL;DR: A global gene expression analysis revealed that the Ath diet up‐regulated the hepatic expression levels of genes for fatty acid synthesis, oxidative stress, inflammation, and fibrogenesis, which were further accelerated by the addition of a high‐fat component.

TL;DR: Findings in hepatocytes indicate that palmitate inhibited insulin signal transduction through JNK activation and that accelerated β-oxidation ofPalmitate caused excess electron flux in the mitochondrial respiratory chain, resulting in increased ROS generation, suggesting mitochondria-derived ROS induced by palmitates may be major contributors to JNKactivation and cellular insulin resistance.

TL;DR: It is noteworthy that transplantation of Ccr5−/− bone marrow was sufficient to protect against impaired glucose tolerance and the effects of loss of CCR5 were related to both reduction of total ATM content and an M2-dominant shift in ATM polarization.