Obesity-Associated Adipose Tissue Inflammation and Transplantation

Abstract

Obesity is often associated with the development of adipose tissue (AT) inflammation, resulting in metabolic dysfunction and an increased risk for developing type 2 diabetes. It is also associated with multiple chronic diseases, including cardiovascular, liver, and kidney disease, and thus can contribute to organ failure. Several studies have investigated whether there is a correlation between obesity and outcomes in transplantation, but there is currently very limited information on the specific role of AT inflammation in the rejection process or on the overall function of the transplanted organ. Here, we provide a brief review of the current understanding of the cellular mechanisms that control obesity-associated AT inflammation and summarize knowledge about how obesity affects clinical outcomes following solid organ or hematopoietic stem cell transplantation. We also highlight opportunities for more research to better understand how obesity affects outcomes of transplantation.

Characterization of regulatory T cells in obese omental adipose tissue in humans

“…B). These data are consistent with the concept that obesity and T2D lead to reduced expression of favorable metabolic genes .…”

“…Indeed, we confirm that obese AT has elevated leptin expression and report the new finding that adiponectin declines in proportion to the degree of obesity and in the presence of T2D. In addition, we found that UCP1 transcript levels in omental AT were lower in patients with T2D, consistent with the idea that in obesity a progressive loss of beige AT and the accumulation of white AT leads to cellular stress in adipocytes, triggering the release of proinflammatory cytokines and ultimately a change in the immune cell composition in AT .…”

“…Visceral AT inflammation in obesity and T2D has been documented in both humans and mice . In humans, although macrophages are known to accumulate in omental AT in severe obesity, there are contradictory results regarding their M1 versus M2 phenotype .…”

“…Conversely, visceral AT in mice fed with a high fat diet is characterized by a reduction in type 2 immune cells and a parallel accumulation of proinflammatory M1 macrophages and cytokines, such as IL‐6, TNF‐α, CCL2, IFN‐γ, and leptin. These inflammatory cytokines are thought to directly contribute to insulin resistance and ultimately the development of T2D .…”

Evolution of Body Composition Following Autologous and Allogeneic Hematopoietic Cell Transplantation: Incidence of Sarcopenia and Association with Clinical Outcomes

“…The reason for this association is unclear and its clinical significance is undetermined. However, we note this in the context of studies that have investigated the impact of obesity-related inflammation on the risk for GVHD [23]. While large retrospective studies evaluating obesity by BMI have not demonstrated a clear association between obesity and GVHD, these studies have not evaluated body composition [24][25][26].…”