Ahmad Aljada

TL;DR: The increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction, which might interfering with the anti-inflammatory effect of insulin, which in turn might promote inflammation.

TL;DR: The original conceptualization of this syndrome was on the basis of resistance to the metabolic actions of insulin, and it was maintained that hyperinsulinemia itself contributes to atherogenicity, and thus, insulin is atherogenic, leading to the coronary heart disease and cerebrovascular disease associated with this syndrome.

TL;DR: It is concluded that endotoxin induces the release of procalcitonin systemically, that this increase is not associated with an increase in calcitonin, and that the increase in procalCitonin associated with septicemia in patients may be mediated through the effect of endotoxin described here.

TL;DR: It is concluded that insulin has a potent acute anti-inflammatory effect including a reduction in intranuclear NFkappaB, an increase in Ikappa B, and decreases in ROS generation, p47(phox) subunit, plasma soluble intercellular adhesion molecule-1, monocyte chemoattractant protein-1 (MCP-1), and plasminogen activator inhibitor- 1 (PAI-1).

TL;DR: It is concluded that glucose intake stimulates ROS generation and p417phox of NADPH oxidase; increases oxidative load and causes a fall in alpha-tocopherol concentration.