The Vicious Cycle of Estrogen Consumption and Obesity: The Role of Mechanotransduction - The Mechanobiology of Obesity and Related Diseases - page 90

addition is often being ignored or less spoken of when discussing the risks
involved in over-consumption of industrialized foods, the potential hazards of
consuming hormonal supplements to foods, particularly diary, chicken and beef,
are not to be underestimated. Estrogen affects, for example, metabolism and
enhances the timing and rate of sexual maturation in both sexes [ 12 , 50 ].
5.2 Estrogen Production in Adipose Tissues
Other than being consumed, estrogen is also being produced by the ovaries and the
adipose tissues [ 50 ]. While the ovaries are the principle sources of estrogen in
premenopausal women, adipose tissues, and specifically, adipose stromal cells are
the major estrogen production sites in postmenopausal women as well as in men
[ 26 , 38 , 70 ]. The activity of the aromatase enzyme dictates the levels of estrogen
since it catalyzes the biosynthesis of estrogen from androgens, thus, it is the rate-
limiting step in estrogen biosynthesis [ 26 , 50 ]. Aromatase expression in adipose
tissues increases with bodyweight and age [ 50 ]. Recent evidence indicates that
increasing matrix compliance can induce the transcription of this enzyme as well
[ 26 ]. The role of estrogen in adipocyte biology includes direct influences on the
proliferation and differentiation of the cells (as described in the next section).
Estrogen also has secondary influences which are induced through the central
nervous system—on leptin secretion and therefore food consumption, and on
energy expenditure through metabolism [ 10 ].
5.3 The Influence of Estrogen on Proliferation
and Differentiation of Adipocytes
The influence of estrogen on proliferation and differentiation of adipocytes seems
to be specie-, gender-, and anatomical site-dependent (Tables 1 and 2 ). For
examples, estrogen was found to significantly promote proliferation of human
primary preadipocytes derived from omental and subcutaneous adipose tissues of
males, post- and pre- menopausal females, and massively obese females [ 2 , 11 , 18 ,
57 ]. Nevertheless, [ 2 ] found that proliferation of cultured omental and subcuta-
neous preadipocytes obtained from females started earlier and increased more
strongly, respectively, with respect to responses of cells from males. Proliferation
of subcutaneous preadipocytes from female rats was found to be stimulated fol-
lowing estrogen exposure as well [ 17 , 41 ]. In contrast, the proliferation of 3T3-L1
mouse preadipocytes was attenuated following exposure to the hormone [ 41 ].
Moreover, mitotic activity of parametrial preadipocytes from male and female rats
as well of epididymal and subcutaneous preadipocytes from male rats was not
significantly affected by the hormone [ 17 ]. Combining these (Table 1 ), estrogen