Abstract

Current research reveals that obesity and adipose tissue growth leads to lipotoxicity resulting in several health perturbations in the human body. Little is known about how the age at which lipid overload starts affects cellular programing in different regions of adipose tissue. In this preliminary study, we hypothesized that the age at which lipotoxicity occurs (age of lipid overload) affects cellular senescence, adipocyte size and number, and preadipocyte proliferation in regional adipose tissue.
We recruited 7 participants with early lipid overload and 13 participants with late lipid overload. Dual x-ray absorptiometry (DXA) and computed tomography (CT) scans were performed to measure body composition. Adipose tissue was collected via biopsy from the abdominal and femoral subcutaneous depots. Adipose tissue was then digested with collagenase. Adipocyte size was determined by digital pictomicrographs. Primary preadipocytes were isolated and cultured from the stromal vascular fraction (SVF) of adipose tissue. Proliferative capacity of cloned preadipocytes was evaluated via DNA quantification using CyQuant dye (Molecular Probes, Inc.) after 5 and 10 passages, while cellular senescence was assessed by β-galactosidase staining.
Regardless of the age of obesity onset, femoral preadipocytes are significantly (p<0.001) more capable of proliferation than abdominal cells at the earlier passages (P5). Moreover, after 5 passages preadipocytes from the femoral depot had greater DNA concentration than they had after 10 passages (p<0.001), whereas DNA concentration in preadipocytes from the abdominal depot did not change across passages. There were no differences in adipocyte size and number between groups, though in general, the abdominal depot had more adipocytes than the femoral subcutaneous adipose tissue depot (p <0.05). There were no differences in cellular senescence between depots or groups.
Taken together, our findings suggest that younger preadipocytes in the femoral depot have better capacity to replicate, create mature adipocytes, support the expansion of SAT and maintain healthy adipose dynamics. The future inclusion of more participants will allow us to draw more solid conclusions as to whether the age at which lipid overload develops affects cellular programming of regional adipose tissue.