Biomedical Engineering Reference
In-Depth Information
Fig. 1 The vicious cycle of
estrogen and obesity.
Consumption and production
of estrogen influence
proliferation and
differentiation of adipocytes,
which consequently changes
the stiffness properties of the
cells and tissues. The resulted
changes in the strain-stress
distributions are very likely to
lead back to: [ 1 ] changes in
aromatase expression and
hence changes in estrogen
production, and [ 2 ] changes
in the proliferation and
differentiation of the cells
Estrogen
production
Estrogen
consumption
Influencing proliferation and
differentiation of adipocytes
Changes in stiffness of adipocytes
Changes in stiffness of adipose tissues
Changes in cell and tissue level
strain-stress distributions
Changes in aromatase expression
9 Closure
This chapter describes the frontier of research in mechanotransduction of adipo-
cytes, suggesting a novel link between estrogen and fat tissues from a biome-
chanical point-of-view. Combining the evidence reviewed here, we surmise that a
feedback spiral coupling the effects of estrogen and mechanotransduction could
exist in WAT, which ultimately leads to development of obesity (Fig. 1 ).
Specifically, estrogen influences lipid accumulation and mitotic activity in adi-
pocytes [ 2 , 11 , 17 , 31 , 35 , 41 , 57 , 82 ]. Hence, the mechanical properties of cells in
the fat tissue are changed under the increased continuous presence of steroid
hormones since mature adipocytes are stiffer than preadipocytes [ 3 , 13 , 67 , 80 , 81 ].
If this process results in higher compliance of the tissue, then synthesis of aro-
matase and consequently of estrogen would be further enhanced in the tissue, and
so forth [ 26 , 50 ]. These structure-function relationships should be examined in
more detail by means of interdisciplinary studies, combining tissue biomechanics,
 
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