Fat, Obesity, and the Endothelium

Abstract

Endothelial cells line all blood vessels in vertebrates. These cells contribute to whole-body nutrient distribution in a variety of ways, including regulation of local blood flow, regulation of trans-endothelial nutrient transport, and paracrine effects. Obesity elicits dramatic whole-body nutrient redistribution, in particular of fat. We briefly review here recent progress on understanding endothelial fat transport; the impact of obesity on the endothelium; and, conversely, how endothelial function can modulate obesity.

Figure 1:

Transport of fatty acids across the endothelium. Free Fatty acids (FFAs) packaged as triglycerides in lipoprotein particles are liberated via lipoprotein lipase (LPL) on the luminal side of the endothelium, anchored by the protein GPIHBP1. FFAs uptake into endothelium is facilitated by fatty acid translocase CD36, on the endoplasmic reticulum, and fatty acid binding proteins (FABPs). fatty acid transport proteins (FATPs) catalyze formation of Acyl-CoAs, which are further processed into the triglyceride pool of lipid droplets. Lipolysis once again liberates FFAs, to be used for fatty acid oxidation or transported to the underlying parenchyma.

Figure 2:

How the endothelium can affect obesity. Left, schematic of thermodynamic contributors to body weight regulation. Right, table outlining recent publications in which endothelial biology is altered, leading to changes in body weight. Effects on adipose tissue angiogenesis, energy expenditure (calories out), fatty acid absorption and food consumption (calories in) highlighted for each study.