The effect of weight-loss surgery in patients with obesity on adipose tissue mesenchymal stem cells versus circulating endothelial progenitor cells.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Obesity imposes dysfunction of the endogenous cellular reparative system, which may manifest as impaired adipose tissue-derived mesenchymal stem/stromal cells (AT-MSCs) function or altered characteristics of circulating endothelial progenitor cells (EPCs). However, whether both systems are abnormal in patients with obesity remains unclear. We hypothesized that human obesity induces impairment of MSCs and EPCs that would be reversed after weight-loss surgery (WLS). Abdominal adipose tissue and peripheral blood mononuclear cells were collected to harvest MSCs and EPCs, respectively, from patients with obesity (n = 8) before and 9-12 months after WLS. MSCs mitochondrial function and EPCs number and surface markers were compared to those collected from healthy controls (HC). Patients with obesity had a higher basal body mass index compared to both HC (P < 0.0001) and post-WLS (P < 0.001). Compared to HC, MSC proliferative and differentiation capacity was preserved (P > 0.05), but they showed at baseline increased mitochondrial oxidative stress, and cytochrome-c release (P < 0.05), with reduced membrane potential and matrix density, which mostly improved after WLS. The percent of circulating CD34 + KDR + CD133 + and CD34 + KDR + EPCs was elevated in patients with obesity (P < 0.05), as were EPC fractions expressing the inflammatory marker VAP-1 or pro-calcinogenic marker OCN-1, yet

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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