Ko Kotani

TL;DR: It is suggested that an increase in MCP-1 expression in adipose tissue contributes to the macrophage infiltration into this tissue, insulin resistance, and hepatic steatosis associated with obesity in mice.

TL;DR: The stable overexpression in a Chinese hamster ovary (CHO) cell line of a mutant p85 alpha (delta p85) protein, which lacks a binding site for p110, disrupted the complex formation between IRS-1 and the catalytic subunit of PI 3-kinase in intact cells during insulin stimulation, suggesting that PI 3 -kinase is required for glucose transport in insulin signaling in CHO cells.

TL;DR: The results suggest that PDE3B is a physiological substrate of Akt and that Akt-mediated phosphorylation of PDE2B on serine-273 is important for insulin-induced activation of Pde3B.

TL;DR: It is suggested that insulin-elicited signals that pass through PI 3-kinase subsequently diverge into at least two independent pathways, an Akt pathway and a PKCλ pathway, and that the latter pathway contributes, at least in part, to insulin stimulation of glucose uptake in 3T3-L1 adipocytes.

TL;DR: The results suggest that the association of IRS‐1 with PI 3‐kinase followed by the activation of PI 3-kinase are required for insulin‐ or IGF‐1‐ induced, but not for EGF‐induced, membrane ruffling.