Estradiol-induced hypophagia is associated with the differential mRNA expression of hypothalamic neuropeptides

Silva, L E C M; Castro, Margaret de; Amaral, Fernando Colbari do; Antunes‐Rodrigues, José; Elias, Lucila Leico Kagohara

doi:10.1590/s0100-879x2010007500059

Cited by 31 publications

(31 citation statements)

References 37 publications

(38 reference statements)

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“…Apart from our work, several research papers revealed a statistically significantly higher food intake in OVX animals compared to intact animals. This effect was often observed in short-term experiments [43][44][45][46], which is in line with our results insofar as the food intake in untreated OVX rats was particularly high during the first half of the experimental period. However, leptin resistance of the used rat strain might explain the more pronounced effect of E2-and Alpha-induced food intake reduction in the present study.…”

Section: Food Intakesupporting

confidence: 93%

Effects of estradiol, estrogen receptor subtype-selective agonists and genistein on glucose metabolism in leptin resistant female Zucker diabetic fatty (ZDF) rats

Weigt

Hertrampf

Flenker

et al. 2015

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Food Intakesupporting

confidence: 93%

Effects of estradiol, estrogen receptor subtype-selective agonists and genistein on glucose metabolism in leptin resistant female Zucker diabetic fatty (ZDF) rats

Weigt

Hertrampf

Flenker

et al. 2015

The Journal of Steroid Biochemistry and Molecular Biology

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“…The ARH also mediates energy balance through NPY and ␤-endorphin. Estradiol is anorexic and has been reported to reduce NPY mRNA in vivo and inhibit NPY release from immortalized hypothalamic neurons (Silva et al, 2010;Dhillon and Belsham, 2011). In terms of feeding regulation, NPY and ␤-endorphin neurons appear to have a parallel organization with both sets of neurons affecting melanin-concentrating hormone neurons in the lateral hypothalamus (Schwartz and Gelling, 2002).…”

Section: Discussionmentioning

confidence: 99%

Membrane-Initiated Estradiol Signaling Induces Spinogenesis Required for Female Sexual Receptivity

Christensen¹,

Dewing²,

Micevych³

2011

J. Neurosci.

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Estrogens have profound actions on the structure of the nervous system during development and in adulthood. One of the signature actions of estradiol is to alter the morphology of neural processes. In the hippocampus, estradiol modulates spines and cellular excitability that affect cognitive behaviors. In the hypothalamus, estradiol increases spine density in mediobasal hypothalamic nuclei that regulate reproduction. The hypothalamic arcuate nucleus (ARH), an important site for modulation of female sexual receptivity, has a sexual dimorphism in dendritic spine density that favors females. In the present study, we used both ␤-actin immunostaining and Golgi staining to visualize estradiol-induced changes in spine density in Long-Evans rats. Golgi impregnation was used to visualize spine shape, and then ␤-actin immunoreactivity was used as a semiquantitative measure of spine plasticity since actin forms the core of dendritic spines. At 4 h after estradiol treatment, both ␤-actin immunofluorescence and filopodial spines were increased (from 70.57 Ϯ 1.09% to 78.01 Ϯ 1.05%, p Ͻ 0.05). Disruption of estradiol-induced ␤-actin polymerization with cytochalasin D attenuated lordosis behavior, indicating the importance of estradiol-mediated spinogenesis for female sexual receptivity (81.43 Ϯ 7.05 to 35.00 Ϯ 11.76, p Ͻ 0.05). Deactivation of cofilin, an actin depolymerizing factor is required for spinogenesis. Membrane-initiated estradiol signaling involving the metabotropic glutamate receptor 1a was responsible for the phosphorylation and thereby deactivation of cofilin. These data demonstrate that estradiolinduced spinogenesis in the ARH is an important cellular mechanism for the regulation of female sexual behavior.

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“…In contrast to the present results with E 2 S, several reports have demonstrated inhibition of NPY by E 2 . E 2 treatment of ovariectomized rats decreased both NPY and AGRP mRNA in the arcuate nucleus (36). Similarly, in rhesus monkeys E 2 decreased AGRP and increased POMC secretion into cerebrospinal fluid (48).…”

Section: Neuropeptides Related To Feeding Behaviormentioning

confidence: 82%

“…The increase of STS levels in the latter stages of gestation suggests an increasing capacity for converting E 2 S to E 2 as the fetus approaches spontaneous parturition. Recent results from this laboratory have indicated that the actions of E 2 S are not identical to those of E 2 (36). It is therefore possible that E 2 S exerts actions that are not ERmediated.…”

Section: Discussionmentioning

confidence: 96%

Genomics of estradiol-3-sulfate action in the ovine fetal hypothalamus

Rabaglino

Richards

Denslow

et al. 2012

Physiological Genomics

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In fetal sheep during late gestation sulfoconjugated estrogens in plasma reach a concentration 40 -100 times greater than unconjugated estrogens. The objective of the present study was to determine the genomics of estradiol-3-sulfate (E2S) action in the ovine fetal brain. The hypothesis was that E2S stimulates genes involved in the neuroendocrine pathways that direct or facilitate fetal development at the end of gestation. Four sets of chronically catheterized ovine twin fetuses were studied (gestational age: 120 -127 days gestation) with one infused with E 2S intracerebroventricularly (1 mg/day) and the other remaining untreated (control). After euthanasia, mRNA samples were extracted from fetal brains. Only hypothalamic samples were employed for this study given the important function of this brain region in the control of the hypothalamus-pituitary-adrenal axis. Microarray analysis was performed following the Agilent protocol for one-color 8 ϫ 15 microarrays, designed for Ovis aries. A total of 363 known genes were significantly upregulated by the E 2S treatment (P Ͻ 0.05). Network and enrichment analyses were performed using the Cytoscape/Bingo software, and the results validated by quantitative realtime PCR. The main overrepresented biological processes resulting from this analysis were feeding behavior, hypoxia response, and transforming growth factor signaling. Notably, the genes involved in the feeding behavior (neuropeptide Y and agouti-related protein) were the most strongly induced by the E2S treatment. In conclusion, E2S may be an important component of the mechanism for activating orexigenic, hypoxia responsiveness and neuroprotective pathways in the lamb as it approaches postnatal life. heart rate; estradiol; hypoxia; estrogen receptor; neuropeptides; neurosteroid IN FETAL SHEEP and pregnant ewes, sulfoconjugated estrogens are far more abundant than unconjugated estrogens (9,41,46). High concentrations of estrone sulfate in uterine vein plasma (compared to peripheral vein plasma) of pregnant sheep suggested a high secretion rate for this steroid by placenta in late gestation (15). Plasma concentrations of estradiol-3-sulfate (E 2 S) are ϳ40 -100 times those of estradiol (E 2 ) in the lategestation fetal sheep. E 2 S is taken up by the fetal brain and stimulates responses that are both similar to and distinct from the responses to E 2 (43, 46). Sulfoconjugation increases the half-life in the blood (33) and supplies a ready source of E 2 in tissues (e.g., hypothalamus) that express steroid sulfatase (STS) (31, 43). E 2 S can bind estrogen receptor only after deconjugation by STS. We have proposed that, while the function of the sulfoconjugated estrogens in fetal and maternal sheep is unknown, deconjugation can increase estrogen action in specific tissues that express STS and estrogen receptor (43,44,46). The fetal brain expresses both STS and estrogen sulfotransferase (STF), allowing for the bidirectional interconversion of E 2 and E 2 S (31, 32), although the ratio of expression for these enzymes fa...

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Estradiol-induced hypophagia is associated with the differential mRNA expression of hypothalamic neuropeptides

Cited by 31 publications

References 37 publications

Effects of estradiol, estrogen receptor subtype-selective agonists and genistein on glucose metabolism in leptin resistant female Zucker diabetic fatty (ZDF) rats

Effects of estradiol, estrogen receptor subtype-selective agonists and genistein on glucose metabolism in leptin resistant female Zucker diabetic fatty (ZDF) rats

Membrane-Initiated Estradiol Signaling Induces Spinogenesis Required for Female Sexual Receptivity

Genomics of estradiol-3-sulfate action in the ovine fetal hypothalamus

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