Estrogen Research Paper

Estrogenic signaling Estrogens are produced in the ovaries, testicals, as well as adipocytes (Schneider, Kirschner et al. 1979, Tchernof, Despres et al. 1995). There are three major naturally occurring forms of estrogen: estrone (E1), estradiol (E2), and estriol (E3). 17 beta-estrodiol is the most prevalent endogenous estrogen. Estrogen enters the cell and passes to the nucleus. Then estrogen binds to a receptor, changing the receptors shape. The estrogen/receptor complex then binds to estrogen response elements (EREs), which are specific DNA sites that are located near genes that are controlled by estrogen. This results in activation or repression of particular gene expression and is affected by the estrogen receptors. ERα is known to be …show more content…
Research in previous studies, using myeloid specific ERα knockouts, has shown that estrogen can alter cytokine and adipokine concentrations, insulin resistance, and increased adipose mass (Ribas, Drew et al. 2011). Ohlsson et al., observed that mice with the ER-α gene knocked out, developed obesity; however, mice with the ER-β gene knocked out did not (Ohlsson, Hellberg et al. 2000). In addition, Dieudonne et al., observed that human adipocytes ER-β mRNA concentrations were considerably lower than ER-α levels (Dieudonne, Leneveu et al. 2004). Human adipocyte nuclear extracts and membrane fractions have been observed to contained ER-α, this suggests that E2 is able to affect human adipocytes similarly to rat adipocytes (Dos Santos, Dieudonne et al. 2002). Other research has suggested that E2 increases the binding of ER to ERE in nuclear proteins from adipocytes, but not preadipocytes, which typically consist of the ER-α subtype (Dieudonne, Leneveu et al. 2004). E2 has also been recognized as a major factor in regulating adipose tissue metabolism in females. (Jeong and Yoon 2011) demonstrated that an OVX in rodents led to weight gain specifically in adipose tissue. The weight gain was reversed by the substitution of physiologic E2 (Jeong, Han et al. 2004, Jeong and Yoon 2007). Lastly, research has shown that obesity …show more content…
Research has previously shown mixed results on whether daidzein inhibits or stimulates adipogenesis (Harmon, Patel et al. 2002, Dang and Lowik 2004, Sakamoto, Naka et al. 2014). Cho et al., demonstrated that based on dose, daidzein can stimulate adipogenesis in 3T3-L1 cells and Pluripotent 10T1/2 cells (Cho, Lee et al. 2010). Daidzein was shown to activate PPARγ-driven reporter-gene activity in differentiated 3T3-L1 cells (Shen, Liu et al. 2006), as well as expression of PPARγ, FABP, and PPARγ transcriptional activity (Cho, Lee et al. 2010). Daidzein, along with increasing differentiation, can increase the insulin stimulated glucose uptake by up-regulation of IRS-1 and GLUT4 expression (Cho, Lee et al. 2010). These increases give rise to the improvement of diabetic symptoms via enhanced glucose uptake and insulin sensitivity. Equol, a daidzein derivative, was found to increase these same factors as daidzein, thus improving diabetic symptoms (Cho, Lee et al.

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