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tscript(p(HGNC:ESR2)) -| bp(MESHPP:Obesity)
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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Estrogens have effects on other organs, such as the liver, that are involved in various aspects of metabolism and that are altered in obesity. For example, estrogen effects on cholesterol uptake, biosynthesis, and catabolism have been documented in the aromatase knockout (ArKO) female, which lacks the enzymatic machinery to make estrogens, although these effects are sexually dimorphic and not seen in ArKO males (39). Relative Roles of ERa and ERb in Adipose Tissue The discovery of a second form of ER, ERb (40), and the demonstration that adipose tissue expressed both ERa and ERb (17) necessitated work to ascertain the relative roles of ERa and ERb in adipose tissue. aERKO mice show over a 100% increase in adipose tissue compared with wild-type (WT) mice (26) (Fig. 3). These increases were similar to those reported concomitantly in ArKO mice (41) and soon afterward in FSH receptor knockout mice (42), both of which do not synthesize E2. These results indicated that loss of E2/ERa signaling in aERKO mice, and the lack of endogenous E2 in the ArKO and FSH receptor knockout mice, which should lead to lack of signaling through both ERa and ERb, led to similar increases in adipose tissue. These results strongly indicate that ERa is the main regulator of estrogen effects on adipose tissue. aERKO mice still express ERb and have tenfold increases in circulating E2 (43), which could cause increased E2/ERb signaling. To evaluate the potential role of E2/ERb signaling in adipose tissue, aERKO mice were ovariectomized to determine whether loss of E2/ERb signaling in animals already lacking E2/ERa signaling induced any demonstrable change in adipose tissue or other parameters. Ovariectomized aERKO mice showed a decrease in adipose tissue and body weight compared to sham-operated aERKO mice, indicating that ERb might have an inhibitory effect on adipose deposition that is opposite that mediated through ERa (19).
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Selventa
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2014-07-03T14:30:29.838+02:00
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