Table 2.
Property | Obesity | Repeated replication | Aging |
---|---|---|---|
Dysdifferentiation | √ | √* | √ |
↑ Inflammation | √ | √ | √ |
↑ TNFα, IL6, MMPs, PAI-1 | √ | √† | √‡ |
Altered progenitor shape | √ | √ | √ |
Insulin resistance | √ | √ | |
↑ Senescence associated β-gal | √§ | √ | √ |
↓β oxidation, PGC-1α | √¶ | √ | |
↑ Stathmin-like-2 (Stmn-2) | √ | √‡ |
Cell dynamic and molecular mechanisms underlying fat tissue dysfunction in obesity in younger individuals are strikingly similar to aging. Similarities between changes in human preadipocyte and fibroblast function after serial passage in vitro to those in preadipocytes from obese or old subjects further support this (Tchkonia et al., 2006b, 2009). Thus, obesity, in some respects, resembles an accelerated form of fat tissue aging, potentially involving fat cell progenitor hyperplasia and cellular stress.
In (Mu & Higgins, 1995).
In (Semple et al., 2004). Other references appear in the text.