Repetitive Postprandial Hypertriglyceridemia Induces Monocyte Adhesion to Aortic Endothelial Cells in Goto-Kakizaki Rats

Abstract

Abstract. To compare the effects of postprandial hypertriglyceridemia and postprandial hyperglycemia on monocyte adhesion to endothelial cells, we investigated the effects of twice-daily standard diet (5% fat) and high-fat diet (30% fat) for 3 weeks on monocyte adhesion to endothelial cells and the expression of adhesion molecules in the aortic artery in nonobese type 2 diabetic Goto-Kakizaki rats. Fasting glucose, insulin, non-esterified fatty acid (NEFA), HbA1c, and body weight were comparable between the two diet groups. Postprandial glucose and insulin were higher in the standard diet group, while postprandial NEFA and triglyceride were higher in the high fat diet group, compared with the other group. The number of monocyte adherent to endothelial cells was higher in the high-fat diet group than the standard diet group. Consumption of high-fat diet resulted in overexpression of heme oxygenase-1, intercellular adhesion molecule-1 (ICAM-1), and connecting segment-1 fibronectin on the arterial wall, compared with standard diet. Thus, our data demonstrated that short-term intermittent high-fat diet prevented postprandial hyperglycemia in a model of type 2 diabetes without a significant increase in body weight. However, the resulting postprandial hypertriglyceridemia induces more monocyte adhesion to endothelial cells than postprandial hyperglycemia. This increased monocyte adhesion is associated with the increased aortic expression of adhesion molecules such as ICAM-1, and connecting segment-1 fibronectin.

Effect of AST-120 on Endothelial Dysfunction in Adenine-Induced Uremic Rats

“…Motojima el al. [25] reported that elevation of ICAM-1, but not VCAM-1 mRNA, was observed in monocyte adhesion in type 2 DM rats fed a high-fat diet. And they reported that the fluctuation in blood glucose enhanced monocyte adhesion to the endothelium in diabetes rats using the NEMOes.…”

Postprandial dysmetabolism: Too early or too late?

“…In addition, experiments in rat models have shown that postprandial hypertriglyceridemia is associated with overexpression of ICAM-1 and increased monocyte adhesion in the aortic arterial wall. 96 Recent data also demonstrate that postprandial hyperglycemia is involved in increased leucocyte activation in patients with type 2 diabetes and familial combined hyperlipidemia. 97 Concerning the coagulation system, there are data demonstrating that postprandial hyperglycemia constitutes a significant predictor of platelet activation, as this was shown by measurement of urinary 11-dehydro-thromboxane (TX)B(2), a marker of in vivo platelet activation, in subjects with type 2 early diabetes.…”

Lipotoxic brain microvascular injury is mediated by activating transcription factor 3-dependent inflammatory and oxidative stress pathways

“…This process results in TGRL remnant particle formation and lipolysis products such as phospholipids and fatty acids. Previous studies have shown that TGRL lipolysis products cause aortic endothelial injury, including inflammation, elevated expression of reactive oxygen species (ROS), and increased vascular permeability (22)(23)(24)(25)(26)(27)(28)(29). Additionally, activating transcription factor (ATF) 3 appears to play an important role as a master regulator of inflammation in the aortic endothelium in response to TGRL lipolysis products (22,30).…”