Abstract
Background: The increase in the incidence of obesity and obesity-related cardiovascular risk factors (CVRFs) over the last decades has brought attention on adipose tissue (AT) pathobiology. The expansion of AT is associated with the development of new vasculature needed to perfuse the tissue; however, not all fat depots have the same ability to induce angiogenesis that requires recruitment of their own endothelial cells. In this study we have investigated the effect of different CVRFs, on the angiogenic capacity of the subcutaneous (SAT) and visceral (VAT) adipose tissue and on the function of their mesenchymal cell reservoir. Methods: A transcriptomic approach was used to compare the different angiogenic and inflammatory profiles of the subcutaneous and visceral fat depots from individuals with obesity, as well as their resident stem cells (ASCs). Influence of other risk factors on fat composition was also measured. Finally, the microvesicles (MVs) released by ASCs were isolated and their regenerative potential analyzed by molecular and cellular methodologies. Results: Obesity decreases the angiogenic capacity of AT. There are differences between SAT and VAT; from the 21 angiogenic-related genes analyzed, only three were decreased in SAT compared with those decreased in VAT. ASCs isolated from both fat depots showed significant differences; there was a significant up-regulation of the VEGF-pathway on visceral derived ASCs. ASCs release MVs that stimulate endothelial cell migration and angiogenic capacity. Conclusions: In patients with obesity, SAT expresses a greater number of angiogenic molecules than VAT, independent of the presence of other CVRFs.
Highlights
Adipose tissue (AT) is widely distributed all around the organism, and constitutes between 15%and 25% of the total body mass; due to its plasticity, it can reach up to 40% of the body mass in individuals with obesity [1,2]
WAT is distributed throughout the body, its principal deposits are in peripheral subcutaneous tissue (SAT) that is present on the hips and thighs, where it functions as an energy storage system, and the visceral or intra-abdominal region (VAT), where it protects against possible trauma
A significant up-regulation of genes involved in inflammation, immunity and cell proliferation was observed in the SAT of obese, compared to individuals with normal weight; advanced glycation end-products (AGER), capping actin protein (CAPG), CD34, CD68, interferon-gamma-inducible protein 30 (IFI30), NOTCH3 AND SPP1 (Table 2; Figure 1B)
Summary
Adipose tissue (AT) is widely distributed all around the organism, and constitutes between 15%and 25% of the total body mass; due to its plasticity, it can reach up to 40% of the body mass in individuals with obesity [1,2]. The ability of adipocytes to buffer dietary lipids declines with age, promoting the redistribution of lipids from subcutaneous to the abdominal visceral compartment [4]. These changes contribute to a low-grade state of inflammation, insulin resistance, and metabolic syndrome, contributing to an increased risk of type 2 diabetes, cardiovascular disease, and many other diseases associated with obesity. CVRFs, on the angiogenic capacity of the subcutaneous (SAT) and visceral (VAT) adipose tissue and on the function of their mesenchymal cell reservoir. Methods: A transcriptomic approach was used to compare the different angiogenic and inflammatory profiles of the subcutaneous and visceral fat depots from individuals with obesity, as well as their resident stem cells (ASCs). The microvesicles (MVs) released by ASCs were isolated and their regenerative potential analyzed by molecular and cellular methodologies
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
