**4. Bariatric surgery impact on subcutaneous ASCs differentiation**

Bariatric surgery is widely acknowledged as the most effective treatment for obesity (Frikke-Schmidt, O'Rourke et al. 2016). The most obvious effect of bariatric surgery is a loss of up to half of the total adipose tissue mass within the first year after surgery along with improvements in systemic metabolism.

Weight loss after bariatric surgery involves extensive remodeling of adipose tissue, comprising the hyperplasia-hypertrophy balance. The bariatric intervention has variable results, with up to 35% of patients achieving suboptimal weight loss [48]. ASC adipogenic potential correlates of metabolic disease and therapeutic responses are poorly defined. Very few published data that correlate changes in weight loss induced by bariatric surgery and preadipocyte functions (**Table 2**).

In obesity, subcutaneous ASCs have abnormal functions in terms of angiogenic differentiation, proliferation, migration, viability, and an altered and inflammatory transcriptome [51, 52]. Weight loss partially rescues some of the aforementioned features.

An important improvement in glycemia is seen in obese patients with diabetes who undergo bariatric surgery, even before clinically significant weight loss occurs. A decrease of 50% in HOMA-IR is seen within 1 week following surgery [53]. Partial or total remission rates in type 2 diabetes as high as 80–90% have been observed to occur following bariatric surgery [54, 55].

Few studies have successfully measured local inflammation within subcutaneous adipose tissues after surgery in human studies. However, these limited findings do indicate that adipose tissue infiltration decreases [56]. A shift in the distribution of the remaining macrophages was also observed, including two features: 1) disappearance of CLS, and 2) macrophages located near blood vessels [56]. The studies that investigated the impact of bariatric surgery on mRNA expression of total macrophage cell marker CD68 in abdominal subcutaneous AT and showed a significant CD68 mRNA expression levels were significantly decreased 12 and 24 months after bariatric surgery but not after 6 months [57–60].

Studies in rodents suggest that although subcutaneous ASCs derived from mice with partial weight loss present an improved proliferative ability, lipid accumulation was lower than in control differentiated ASCs. The inefficient lipid storage could indicate that after weight loss, ASCs do not recover the ability to differentiate *Subcutaneous Adipose Stem Cells in Obesity: The Impact of Bariatric Surgery DOI: http://dx.doi.org/10.5772/intechopen.95542*


**Table 2.**

*Relationship between subcutaneous ASCs and weight loss induced by surgical interventions.*

to the adipocyte lineage. These studies indicate that reduced energy intake might create a protective environment [37].

Mitterberger et al. [49] provided evidence suggesting that long-term caloric restriction-induced by diet and bariatric surgery reduced DNA-damage, improved viability, extended replicative lifespan, and reduced adipogenic differentiation potential of subcutaneous ASCs in formerly obese women.

Muir et al. [48] observed a relationship between pre-surgical subcutaneous ASCs frequency and surgery-induced weight loss only in women, suggesting different sex-specific mechanisms of tissue remodeling associated with bariatric surgery weight loss responses. [48]. These findings indicate that the diagnosis of ASCs functions pre-bariatric surgery could predict the level of metabolic changes following bariatric surgery. This data would allow specialists to establish some criteria for the selection of obese patients with metabolic comorbidities for whom bariatric surgery would have the greatest benefit.
