Postprandial Mononuclear NF-κB Activation is Independent of the AGE-content of a Single Meal

Abstract

Postprandial mononuclear NF-kappaB activation after a single meal is independent of the AGE-content of the ingested protein.

Effect of Acarbose on Postmeal Mononuclear Blood Cell Response in Patients with Early Type 2 Diabetes: The AI(I)DA Study

“…It could be assumed that these lymphocytes may be derived from Peyer plaques along the small intestine. As shown by Schiekofer et al [18] a mixed meal in patients with type 2 diabetes leads to activation of Nf κ B receptors of mononuclear cells of the blood. This activation of a central proinfl ammatory pathway can be blocked by acarbose [9] .…”

The mechanism by which dietary AGEs are a risk to human health is via their interaction with RAGE: Arguing against the motion

“…Recent studies indicate that food intake results in an increase in serum AGEs and dicarbonyls within a short time [19,20]. One could argue that these might represent secondary AGEs formed intracellularly as a consequence of postprandial inflammatory reactions because these AGEs have been shown to be ligands of RAGE and to effectively modulate RAGE-dependent gene expression and vascular dysfunction.…”

“…Schiekofer et al [20] fed casein glycated by sorbitol or glucose to volunteers. The use of the different sugars resulted in significantly higher CML and pentosidine contents in the glucose-treated casein.…”

The anti‐adipogenic effect of peripheral blood mononuclear cells is absent with PCSK9 loss‐of‐function variants

“…Effects of an oral fat load on PBMC activation and metabolism have been studied previously, mainly on monocytes. They show increased cellular lipid content, more nuclear factor‐κB activation, and higher expression of apoB48R and CD11b . Our data show that, after a fat load, the only change in gene expression was an increase in MCP‐1 mRNA levels in PBMC from the non‐variant controls.…”