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Article ; Online: The loss of ERE-dependent ERα signaling potentiates the effects of maternal high-fat diet on energy homeostasis in female offspring fed an obesogenic diet.

Roepke, Troy A / Yasrebi, Ali / Villalobos, Alejandra / Krumm, Elizabeth A / Yang, Jennifer A / Mamounis, Kyle J

Journal of developmental origins of health and disease

2019 Volume 11, Issue 3, Page(s) 285–296

Abstract: Maternal high-fat diet (HFD) alters hypothalamic programming and disrupts offspring energy homeostasis in rodents. We previously reported that the loss of ERα signaling partially blocks the effects of maternal HFD in female offspring fed a standard chow ... ...

Abstract	Maternal high-fat diet (HFD) alters hypothalamic programming and disrupts offspring energy homeostasis in rodents. We previously reported that the loss of ERα signaling partially blocks the effects of maternal HFD in female offspring fed a standard chow diet. In a companion study, we determined if the effects of maternal HFD were magnified by an adult obesogenic diet in our transgenic mouse models. Heterozygous ERα knockout (wild-type (WT)/KO) dams were fed a control breeder chow diet (25% fat) or a semipurified HFD (45% fat) 4 weeks prior to mating with heterozygous males (WT/KO or WT/ knockin) to produce WT, ERα KO, or ERα knockin/knockout (KIKO) (no estrogen response element (ERE) binding) female offspring, which were fed HFD for 20 weeks. Maternal HFD potentiated the effects of adult HFD on KIKO and KO body weight due to increased adiposity and decreased activity. Maternal HFD also produced KIKO females that exhibit KO-like insulin intolerance and impaired glucose homeostasis. Maternal HFD increased plasma interleukin 6 and monocyte chemoattractant protein 1 levels and G6pc and Pepck liver expression only in WT mice. Insulin and tumor necrosis factor α levels were higher in KO offspring from HFD-fed dams. Arcuate and liver expression of Esr1 was altered in KIKO and WT, respectively. These data suggest that loss of ERE-dependent ERα signaling, and not total ERα signaling, sensitizes females to the deleterious influence of maternal HFD on offspring energy and glucose potentially through the control of peripheral inflammation and hypothalamic and liver gene expression. Future studies will interrogate the tissue-specific mechanisms of maternal HFD programming through ERα signaling.
MeSH term(s)	Animals ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Energy Metabolism/genetics ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genetic Predisposition to Disease ; Humans ; Infant ; Infant Nutritional Physiological Phenomena ; Male ; Maternal Nutritional Physiological Phenomena ; Mice ; Mice, Knockout ; Obesity/etiology ; Response Elements ; Sex Factors ; Signal Transduction/genetics
Chemical Substances	Esr1 protein, mouse ; Estrogen Receptor alpha
Language	English
Publishing date	2019-09-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2554780-X
ISSN	2040-1752 ; 2040-1744
ISSN (online)	2040-1752
ISSN	2040-1744
DOI	10.1017/S2040174419000515
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Arcuate Estrogen-Regulated Transcriptome: Estrogen Response Element-Dependent and -Independent Signaling of ERα in Female Mice.

Yang, Jennifer A / Stires, Hillary / Belden, William J / Roepke, Troy A

Endocrinology

2017 Volume 158, Issue 3, Page(s) 612–626

Abstract: To influence energy homeostasis and reproduction, 17β-estradiol (E2) controls the arcuate nucleus (ARC) through multiple receptor-mediated mechanisms, but primarily via estrogen receptor (ER) α, which signals through both estrogen response element (ERE)- ... ...

Abstract	To influence energy homeostasis and reproduction, 17β-estradiol (E2) controls the arcuate nucleus (ARC) through multiple receptor-mediated mechanisms, but primarily via estrogen receptor (ER) α, which signals through both estrogen response element (ERE)-dependent and -independent mechanisms. To determine ERα-mediated, ERE-dependent, and ERE-independent E2 signaling in the ARC, we examined the differential regulation of the mouse arcuate transcriptome by E2 using three mice genotypes: (1) wild-type, (2) ERα knock-in/knockout (ERE-independent mechanisms), and (3) total ERα knockout (ERα-independent mechanisms). Females were ovariectomized and injected with oil or E2, and RNA sequencing on the ARC was used to identify E2-regulated genes in each genotype. Our results show that E2 regulates numerous genes involved in cell signaling, cytoskeleton structure, inflammation, neurotransmission, neuropeptide production, and transcription. Furthermore, ERE-independent signaling regulates ARC genes expressed in kisspeptin neurons and transcription factors that control the hypothalamic/pituitary/gonadal axis. Interestingly, a few genes involved in mitochondrial oxidative respiration were regulated by E2 through ERα-independent signaling. A comparison within oil- and E2-treated females across the three genotypes suggests that genes involved in cell growth and proliferation, extracellular matrices, neuropeptides, receptors, and transcription are differentially expressed across the genotypes. Comparing with previously published chromatin immunoprecipitation sequencing analysis, we found that ERE-independent regulation in the ARC is mainly mediated by tethering of ERα, which is consistent with previous findings. We conclude that the mouse arcuate estrogen-regulated transcriptome is regulated by multiple receptor-mediated mechanisms to modulate the central control of energy homeostasis and reproduction, including novel E2-responsive pathways.
MeSH term(s)	Animals ; Arcuate Nucleus of Hypothalamus/metabolism ; Estradiol/metabolism ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Neuropeptides/metabolism ; Polymerase Chain Reaction ; Response Elements ; Signal Transduction ; Transcriptome
Chemical Substances	Estrogen Receptor alpha ; Neuropeptides ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2017--01
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2016-1663
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Article ; Online: Stress rapidly suppresses in vivo LH pulses and increases activation of RFRP-3 neurons in male mice

Yang, Jennifer A / Hughes, Jessica K / Parra, Ruby A / Volk, Katrina M / Kauffman, Alexander S

The Journal of endocrinology

2018 Volume 239, Issue 3, Page(s) 339–350

Abstract: Restraint stress is a psychosocial stressor that suppresses reproductive status, including LH pulsatile secretion, but the neuroendocrine mechanisms underlying this inhibition remains unclear. Reproductive neural populations upstream of gonadotropin- ... ...

Abstract	Restraint stress is a psychosocial stressor that suppresses reproductive status, including LH pulsatile secretion, but the neuroendocrine mechanisms underlying this inhibition remains unclear. Reproductive neural populations upstream of gonadotropin-releasing hormone (GnRH) neurons, such as kisspeptin, neurokinin B and RFRP-3 (GnIH) neurons, are possible targets for psychosocial stress to inhibit LH pulses, but this has not been well examined, especially in mice in which prior technical limitations prevented assessment of in vivo LH pulse secretion dynamics. Here, we examined whether one-time acute restraint stress alters in vivo LH pulsatility and reproductive neural populations in male mice, and what the time-course is for such alterations. We found that endogenous LH pulses in castrated male mice are robustly and rapidly suppressed by one-time, acute restraint stress, with suppression observed as quickly as 12–18 min. This rapid LH suppression parallels with increased in vivo corticosterone levels within 15 min of restraint stress. Although Kiss1, Tac2 and Rfrp gene expression in the hypothalamus did not significantly change after 90 or 180 min restraint stress, arcuate Kiss1 neural activation was significantly decreased after 180 min. Interestingly, hypothalamic Rfrp neuronal activation was strongly increased at early times after restraint stress initiation, but was attenuated to levels lower than controls by 180 min of restraint stress. Thus, the male neuroendocrine reproductive axis is quite sensitive to short-term stress exposure, with significantly decreased pulsatile LH secretion and increased hypothalamic Rfrp neuronal activation occurring rapidly, within minutes, and decreased Kiss1 neuronal activation also occurring after longer stress durations.
MeSH term(s)	Animals ; Corticosterone/blood ; Kisspeptins/metabolism ; Luteinizing Hormone/metabolism ; Male ; Mice, Inbred C57BL ; Neuropeptides/metabolism ; Neurosecretory Systems/metabolism ; Protein Precursors/metabolism ; Stress, Psychological/metabolism ; Tachykinins/metabolism
Chemical Substances	Kiss1 protein, mouse ; Kisspeptins ; Neuropeptides ; Protein Precursors ; RFamide peptide ; Tachykinins ; preprotachykinin ; Luteinizing Hormone (9002-67-9) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2018-10-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3028-4
ISSN	1479-6805 ; 0022-0795
ISSN (online)	1479-6805
ISSN	0022-0795
DOI	10.1530/JOE-18-0449
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Article ; Online: Regulation of gene expression by 17β-estradiol in the arcuate nucleus of the mouse through ERE-dependent and ERE-independent mechanisms.

Yang, Jennifer A / Mamounis, Kyle J / Yasrebi, Ali / Roepke, Troy A

Steroids

2016 Volume 107, Page(s) 128–138

Abstract: 17β-Estradiol (E2) modulates gene expression in the hypothalamic arcuate nucleus (ARC) to control homeostatic functions. In the ARC, estrogen receptor (ER) α is highly expressed and is an important contributor to E2's actions, controlling gene expression ...

Abstract	17β-Estradiol (E2) modulates gene expression in the hypothalamic arcuate nucleus (ARC) to control homeostatic functions. In the ARC, estrogen receptor (ER) α is highly expressed and is an important contributor to E2's actions, controlling gene expression through estrogen response element (ERE)-dependent and -independent mechanisms. The objective of this study was to determine if known E2-regulated genes are regulated through these mechanisms. The selected genes have been shown to regulate homeostasis and have been separated into three subsections: channels, receptors, and neuropeptides. To determine if ERE-dependent or ERE-independent mechanisms regulate gene expression, two transgenic mouse models, an ERα knock-out (ERKO) and an ERα knock-in/knock-out (KIKO), which lacks a functional ERE binding domain, were used in addition to their wild-type littermates. Females of all genotypes were ovariectomized and injected with oil or estradiol benzoate (E2B). Our results suggest that E2B regulates multiple genes through these mechanisms. Of note, Cacna1g and Kcnmb1 channel expression was increased by E2B in WT females only, suggesting an ERE-dependent regulation. Furthermore, the NKB receptor, Tac3r, was suppressed by E2B in WT and KIKO females but not ERKO females, suggesting that ERα-dependent, ERE-independent signaling is necessary for Tac3r regulation. The adrenergic receptor Adra1b was suppressed by E2B in all genotypes indicating that ERα is not the primary receptor for E2B's actions. The neuropeptide Tac2 was suppressed by E2B through ERE-dependent mechanisms. These results indicate that E2B activates both ERα-dependent and independent signaling in the ARC through ERE-dependent and ERE-independent mechanisms to control gene expression.
MeSH term(s)	Animals ; Arcuate Nucleus of Hypothalamus/metabolism ; Estradiol/pharmacology ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Gene Knock-In Techniques ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism
Chemical Substances	Estrogen Receptor alpha ; Nerve Tissue Proteins ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80312-1
ISSN	1878-5867 ; 0039-128X
ISSN (online)	1878-5867
ISSN	0039-128X
DOI	10.1016/j.steroids.2016.01.003
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Zs.A 87: Show issues

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Article ; Online: The interaction of fasting, caloric restriction, and diet-induced obesity with 17β-estradiol on the expression of KNDy neuropeptides and their receptors in the female mouse.

Yang, Jennifer A / Yasrebi, Ali / Snyder, Marisa / Roepke, Troy A

Molecular and cellular endocrinology

2016 Volume 437, Page(s) 35–50

Abstract: Arcuate neurons that coexpress kisspeptin (Kiss1), neurokinin B (Tac2), and dynorphin (Pdyn) mediate negative feedback of 17β-estradiol (E2) on the HPG axis. Previous studies report that fasting and caloric restriction reduce arcuate Kiss1 expression. ... ...

Abstract	Arcuate neurons that coexpress kisspeptin (Kiss1), neurokinin B (Tac2), and dynorphin (Pdyn) mediate negative feedback of 17β-estradiol (E2) on the HPG axis. Previous studies report that fasting and caloric restriction reduce arcuate Kiss1 expression. The objective of this study was to determine the interactions of E2 with fasting, caloric restriction, and diet-induced obesity on KNDy gene and receptor expression. Ovariectomized female mice were separated into control and estradiol benzoate (E2B)-treated groups. E2B decreased Kiss1 and the tachykinin 2 receptor, Tac3r, in ARC tissue and Tac2 in Tac2 neurons. Diet-induced obesity decreased Kiss1 in oil-treated animals and the kisspeptin receptor, Kiss1r and Tac3r in the ARC of E2B-treated animals. Chronic caloric (30%) restriction reduced all three neuropeptides in oil-treated females and Kiss1r by E2B in CR animals. Taken together, our experiments suggest that steroidal environment and energy state negatively regulate KNDy gene expression in both ARC and Tac2 neurons.
MeSH term(s)	Animals ; Arcuate Nucleus of Hypothalamus/metabolism ; Body Composition ; Body Weight ; Caloric Restriction ; Diet ; Diet, High-Fat ; Dynorphins/genetics ; Dynorphins/metabolism ; Estradiol/blood ; Estradiol/metabolism ; Estradiol/pharmacology ; Fasting ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Ghrelin/metabolism ; Kisspeptins/genetics ; Kisspeptins/metabolism ; Mice, Inbred C57BL ; Models, Biological ; Neurokinin B/genetics ; Neurokinin B/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Neuropeptides/genetics ; Neuropeptides/metabolism ; Obesity/blood ; Obesity/genetics ; Obesity/metabolism ; Organ Size ; Signal Transduction/drug effects ; Signal Transduction/genetics
Chemical Substances	Ghrelin ; Kisspeptins ; Neuropeptides ; Estradiol (4TI98Z838E) ; Dynorphins (74913-18-1) ; Neurokinin B (86933-75-7)
Language	English
Publishing date	2016-08-06
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2016.08.008
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Zs.A 1127: Show issues

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Article ; Online: Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice.

Roepke, Troy A / Yasrebi, Ali / Villalobos, Alejandra / Krumm, Elizabeth A / Yang, Jennifer A / Mamounis, Kyle J

Scientific reports

2017 Volume 7, Issue 1, Page(s) 6381

Abstract: Maternal high-fat diet (HFD) alters hypothalamic developmental programming and disrupts offspring energy homeostasis in rodents. 17β-estradiol (E2) also influences hypothalamic programming through estrogen receptor (ER) α. Therefore, we hypothesized that ...

Abstract	Maternal high-fat diet (HFD) alters hypothalamic developmental programming and disrupts offspring energy homeostasis in rodents. 17β-estradiol (E2) also influences hypothalamic programming through estrogen receptor (ER) α. Therefore, we hypothesized that females lacking ERα would be more susceptible to maternal HFD. To address this question, heterozygous ERα knockout (WT/KO) dams were fed a control breeder chow diet (25% fat) or a semi-purified HFD (45% fat) 4 weeks prior to mating with WT/KO males or heterozygous males with an ERα DNA-binding domain mutation knocked in (WT/KI) to produce WT, ERα KO, or ERα KIKO females lacking ERE-dependent ERα signaling. Maternal HFD increased body weight in WT and KIKO, in part, due to increased adiposity and daytime carbohydrate utilization in WT and KIKO, while increasing nighttime fat utilization in KO. Maternal HFD also increased plasma leptin, IL-6, and MCP-1 in WT and increased arcuate expression of Kiss1 and Esr1 (ERα) and liver expression of G6pc and Pepck in WT and KIKO. Contrary to our hypothesis, these data suggest that loss of ERα signaling blocks the influence of maternal HFD on energy homeostasis, inflammation, and hypothalamic and liver gene expression and that restoration of ERE-independent ERα signaling partially reestablishes susceptibility to maternal HFD.
MeSH term(s)	Animals ; Body Weight ; Chemokine CCL2/metabolism ; Diet, High-Fat/adverse effects ; Estradiol/chemistry ; Estradiol/genetics ; Estradiol/metabolism ; Estrogen Receptor alpha/chemistry ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Gene Knockout Techniques ; Homeostasis ; Interleukin-6/metabolism ; Leptin/blood ; Male ; Mice ; Mutation ; Pregnancy ; Prenatal Exposure Delayed Effects/chemically induced ; Prenatal Exposure Delayed Effects/genetics ; Prenatal Exposure Delayed Effects/metabolism ; Sex Factors ; Signal Transduction
Chemical Substances	Ccl2 protein, mouse ; Chemokine CCL2 ; Estrogen Receptor alpha ; Interleukin-6 ; Leptin ; interleukin-6, mouse ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2017-07-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-06560-x
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Article ; Online: Activation of Estrogen Response Element-Independent ERα Signaling Protects Female Mice From Diet-Induced Obesity.

Yasrebi, Ali / Rivera, Janelle A / Krumm, Elizabeth A / Yang, Jennifer A / Roepke, Troy A

Endocrinology

2017 Volume 158, Issue 2, Page(s) 319–334

Abstract: 17β-estradiol (E2) regulates central and peripheral mechanisms that control energy and glucose homeostasis predominantly through estrogen receptor α (ERα) acting via receptor binding to estrogen response elements (EREs). ERα signaling is also involved in ...

Abstract	17β-estradiol (E2) regulates central and peripheral mechanisms that control energy and glucose homeostasis predominantly through estrogen receptor α (ERα) acting via receptor binding to estrogen response elements (EREs). ERα signaling is also involved in mediating the effects of E2 on diet-induced obesity (DIO), although the roles of ERE-dependent and -independent ERα signaling in reducing the effects of DIO remain largely unknown. We hypothesize that ERE-dependent ERα signaling is necessary to ameliorate the effects of DIO. We addressed this question using ERα knockout (KO) and ERα knockin/knockout (KIKO) female mice, the latter expressing an ERα that lacks a functional ERE binding domain. Female mice were ovariectomized, fed a low-fat diet (LFD) or a high-fat diet (HFD), and orally dosed with vehicle or estradiol benzoate (EB) (300 μg/kg). After 9 weeks, body composition, glucose and insulin tolerance, peptide hormone and inflammatory cytokine levels, and hypothalamic arcuate nucleus and liver gene expression were assessed. EB reduced body weight and body fat in wild-type (WT) female mice, regardless of diet, and in HFD-fed KIKO female mice, in part by reducing energy intake and feeding efficiency. EB reduced fasting glucose levels in KIKO mice fed both diets but augmented glucose tolerance only in HFD-fed KIKO female mice. Plasma insulin and interleukin 6 were elevated in KIKO and KO female mice compared with LFD-fed WT female mice. Expression of arcuate neuropeptide and receptor genes and liver fatty acid biosynthesis genes was altered by HFD and by EB through ERE-dependent and -independent mechanisms. Therefore, ERE-independent signaling mechanisms in both the brain and peripheral organs mediate, in part, the effects of E2 during DIO.
MeSH term(s)	Adiposity ; Animals ; Arcuate Nucleus of Hypothalamus/drug effects ; Arcuate Nucleus of Hypothalamus/metabolism ; Body Weight ; Cytokines/metabolism ; Diet, High-Fat/adverse effects ; Eating/drug effects ; Estradiol/metabolism ; Estradiol/pharmacology ; Estradiol/therapeutic use ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation ; Glucose/metabolism ; Homeostasis ; Liver/drug effects ; Liver/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity/etiology ; Obesity/metabolism ; Obesity/prevention & control ; Response Elements
Chemical Substances	Cytokines ; Estrogen Receptor alpha ; Estradiol (4TI98Z838E) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2017--01
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2016-1535
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Article: The interaction of fasting, caloric restriction, and diet-induced obesity with 17β-estradiol on the expression of KNDy neuropeptides and their receptors in the female mouse

Yang, Jennifer A / Roepke, Troy A / Snyder, Marisa / Yasrebi, Ali

Molecular and Cellular Endocrinology. 2016 Dec. 05, v. 437

2016

Abstract	Arcuate neurons that coexpress kisspeptin (Kiss1), neurokinin B (Tac2), and dynorphin (Pdyn) mediate negative feedback of 17β-estradiol (E2) on the HPG axis. Previous studies report that fasting and caloric restriction reduce arcuate Kiss1 expression. The objective of this study was to determine the interactions of E2 with fasting, caloric restriction, and diet-induced obesity on KNDy gene and receptor expression. Ovariectomized female mice were separated into control and estradiol benzoate (E2B)-treated groups. E2B decreased Kiss1 and the tachykinin 2 receptor, Tac3r, in ARC tissue and Tac2 in Tac2 neurons. Diet-induced obesity decreased Kiss1 in oil-treated animals and the kisspeptin receptor, Kiss1r and Tac3r in the ARC of E2B-treated animals. Chronic caloric (30%) restriction reduced all three neuropeptides in oil-treated females and Kiss1r by E2B in CR animals. Taken together, our experiments suggest that steroidal environment and energy state negatively regulate KNDy gene expression in both ARC and Tac2 neurons.
Keywords	energy ; estradiol ; fasting ; females ; gene expression ; genes ; low calorie diet ; mice ; neurons ; neuropeptides ; obesity ; ovariectomy ; receptors
Language	English
Dates of publication	2016-1205
Size	p. 35-50.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2016.08.008
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 1127: Show issues

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Article ; Online: Estrogen response element-independent signaling partially restores post-ovariectomy body weight gain but is not sufficient for 17β-estradiol's control of energy homeostasis.

Mamounis, Kyle J / Yang, Jennifer A / Yasrebi, Ali / Roepke, Troy A

Steroids

2013 Volume 81, Page(s) 88–98

Abstract: The steroid 17β-estradiol (E2) modulates energy homeostasis by reducing feeding behavior and increasing energy expenditure primarily through estrogen receptor α (ERα)-mediated mechanisms. Intact ERαKO female mice develop obesity as adults exhibiting ... ...

Abstract	The steroid 17β-estradiol (E2) modulates energy homeostasis by reducing feeding behavior and increasing energy expenditure primarily through estrogen receptor α (ERα)-mediated mechanisms. Intact ERαKO female mice develop obesity as adults exhibiting decreased energy expenditure and increased fat deposition. However, intact transgenic female mice expressing a DNA-binding-deficient ERα (KIKO) are not obese and have similar energy expenditure, activity and fat deposition as to wild type (WT) females, suggesting that non-estrogen response element (ERE)-mediated signaling is important in E2 regulation of energy homeostasis. Initial reports did not examine the effects of ovariectomy on energy homeostasis or E2's attenuation of post-ovariectomy body weight gain. Therefore, we sought to determine if low physiological doses of E2 (250 ng QOD) known to suppress post-ovariectomy body weight gain in WT females would suppress body weight gain in ovariectomized KIKO females. We observed that the post-ovariectomy increase in body weight was significantly greater in WT females than in KIKO females. Furthermore, E2 did not significantly attenuate the body weight gain in KIKO females as it did in WT females. E2 replacement suppressed food intake and fat accumulation while increasing nighttime oxygen consumption and activity only in WT females. E2 replacement also increased arcuate POMC gene expression in WT females only. These data suggest that in the intact female, ERE-independent mechanisms are sufficient to maintain normal energy homeostasis and to partially restore the normal response to ovariectomy. However, they are not sufficient for E2's suppression of post-ovariectomy body weight gain and its effects on metabolism and activity.
MeSH term(s)	Animals ; Body Composition/drug effects ; Eating/drug effects ; Energy Metabolism/genetics ; Estradiol/blood ; Estradiol/pharmacology ; Estrogen Receptor alpha/genetics ; Estrogens/metabolism ; Female ; Gene Expression Regulation ; Homeostasis ; Mice ; Mice, Transgenic ; Ovariectomy ; Pro-Opiomelanocortin/genetics ; Response Elements ; Uterus/drug effects ; Weight Gain/drug effects
Chemical Substances	Estrogen Receptor alpha ; Estrogens ; Estradiol (4TI98Z838E) ; Pro-Opiomelanocortin (66796-54-1)
Language	English
Publishing date	2013-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80312-1
ISSN	1878-5867 ; 0039-128X
ISSN (online)	1878-5867
ISSN	0039-128X
DOI	10.1016/j.steroids.2013.10.018
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 87: Show issues

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Article ; Online: Acute Psychosocial Stress Inhibits LH Pulsatility and Kiss1 Neuronal Activation in Female Mice.

Yang, Jennifer A / Song, Christopher I / Hughes, Jessica K / Kreisman, Michael J / Parra, Ruby A / Haisenleder, Daniel J / Kauffman, Alexander S / Breen, Kellie M

Endocrinology

2017 Volume 158, Issue 11, Page(s) 3716–3723

Abstract: Psychosocial stress, such as isolation and restraint, disrupts reproductive neuroendocrine activity. Here we investigate the impact of psychosocial stress on luteinizing hormone (LH) pulses and gene expression and neuronal activation within Rfrp and ... ...

Abstract	Psychosocial stress, such as isolation and restraint, disrupts reproductive neuroendocrine activity. Here we investigate the impact of psychosocial stress on luteinizing hormone (LH) pulses and gene expression and neuronal activation within Rfrp and Kiss1 cells in female mice. Mice were ovariectomized (OVX) and handled daily to habituate to the tail-tip blood collection procedure. Blood was collected every 5 minutes for 180 minutes for measurement of LH. After 90 minutes, stress animals were placed into restraint devices and isolated to new cages. No-stress control animals remained in their home cages. LH pulses occurred at regular intervals during the entire 180-minute sampling period in controls. In contrast, stress induced a rapid and robust suppression of pulsatile LH secretion. Stress reduced the frequency of pulses by 60% and diminished basal LH levels by 40%; pulse amplitude was unaffected. In a separate cohort of OVX females, brains were collected after 45, 90, or 180 minutes of stress or in no-stress controls. At all time points, stress induced a potent decrease in arcuate Kiss1 neuronal activation, using cfos induction as a marker, with a 50% to 60% suppression vs control levels, whereas Rfrp and cfos coexpression in the dorsal-medial nucleus was elevated after 45 minutes of stress. Although arcuate Kiss1 gene expression remained stable, Rfrp expression was elevated 20% after 180 minutes of stress. These findings demonstrate rapid suppression of LH pulsatile secretion by psychosocial stress, associated with reduced cfos induction in Kiss1 neurons and time-dependent increases in Rfrp neuronal activation and messenger RNA.
MeSH term(s)	Acute Disease ; Animals ; Female ; Gene Expression ; Kisspeptins/metabolism ; Luteinizing Hormone/blood ; Luteinizing Hormone/genetics ; Luteinizing Hormone/secretion ; Mice ; Mice, Inbred C57BL ; Neurons/metabolism ; Neurons/physiology ; Neuropeptides/metabolism ; Stress, Psychological/blood ; Stress, Psychological/metabolism
Chemical Substances	Kiss1 protein, mouse ; Kisspeptins ; Neuropeptides ; RFamide peptide ; Luteinizing Hormone (9002-67-9)
Language	English
Publishing date	2017-09-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2017-00301
Database	MEDical Literature Analysis and Retrieval System OnLINE

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