Abstract
Obesity-related comorbidities are, in large part, originated from the dysfunction of adipose tissue. Most of them revert after the normalization of body mass. Adipose tissue is essentially occupied by adipocytes. However, different populations of immunological cells and adipocyte precursor cells (AdPCs) are the main cellular components of tissue. During obesity, body fat depots acquire a low-level chronic inflammation and adipocytes increase in number and volume. Conversely, weight loss improves the inflammatory phenotype of adipose tissue immune cells and reduces the volume of adipocytes. Nevertheless, very little is known about the evolution of the human AdPCs reservoir. We have developed a flow cytometry-based methodology to simultaneously quantify the main cell populations of adipose tissue. Starting from this technical approach, we have studied human adipose tissue samples (visceral and subcutaneous) obtained at two different physiological situations: at morbid obesity and after bariatric surgery-induced weight loss. We report a considerable increase of the AdPCs reservoir after losing weight and several changes in the immune cells populations of adipose tissue (mast cells increase, neutrophils decrease and macrophages switch phenotype). No changes were observed for T-lymphocytes, which are discussed in the context of recent findings.
Highlights
The incidence of obesity is rising dramatically
The only way to generate new adipocytes is through the activation of self-renewing adipocyte precursor cells (AdPCs)
In adult subjects, adipose tissue would expand preferably because of adipocyte hypertrophy, while AdPCs activation would be restricted to the reposition of death adipocytes[22]
Summary
The incidence of obesity is rising dramatically This in turn increases the risk of developing type II diabetes, fatty liver disease and cardiovascular disease. It is associated with other pathologies such as cancer, immune disorders and psychiatric disturbances[1,2,3]. Adipose tissue cells acquire a chronic proinflammatory phenotype[10,11] and adipocytes increase in number and volume[12,13]. The state of low-level chronic inflammation, promoted by obesity at fat depots, begins to reverse a few months after surgery-induced weight loss[18]. This study aims to explore tissue remodelling, at cell level, in the context of weight loss induced by bariatric surgery
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