Sanshiro Tateya

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 results suggest that FSP27 contributes to efficient energy storage in WAT by promoting the formation of unilocular lipid droplets, thereby restricting lipolysis and finding that the nature of lipid accumulation in Wat appears to be associated with maintenance of energy balance and insulin sensitivity.

TL;DR: Molecular mechanisms relevant to the pathophysiology of obesity-induced insulin resistance are introduced and the most recent studies of clinical applications targeting chronic inflammation are reviewed.

TL;DR: An increase in the concentration of MCP-1 in the circulation is sufficient to induce systemic insulin resistance irrespective of adipose tissue inflammation, and inhibition of signaling by M CP-1 and its receptor CCR2 by administration of a novel C CR2 antagonist ameliorated insulin resistance in mice fed a high-fat diet.

TL;DR: It is shown that high-fat feeding induces proinflammatory activation of Kupffer cells in wild-type mice coincident with reduced liver endothelial nitric oxide synthase activity and NO content while enhancement of signaling downstream of endogenous NO by phosphodiesterase-5 inhibition protects against high fat–induced inflammation in K upffer cells.