17β-estradiol modulates the activity of D2 receptors in the regulation of food intake and body weight. The functional lack of 17β-estradiol in postmenopausal women could create a dietary imbalance and cause body wei...17β-estradiol modulates the activity of D2 receptors in the regulation of food intake and body weight. The functional lack of 17β-estradiol in postmenopausal women could create a dietary imbalance and cause body weight gain. This study aimed to better understand the interferences that could exist between 17β-estradiol, D2 receptors and the selection of carbohydrate, fat and protein consumption, as well as their consequences on body weight gain by using an animal model of the menopause. Ovariectomy exacerbates the consumption of foods rich in lipids. Thus confirming an inhibitory action of 17β-estradiol (E2) on the consumption of these types of foods. This consumption stimulates body weight gain, which is promoted by the high caloric content of these foods and not by the amount consumed. Our results showed a direct involvement of D2 receptors in food choice. This choice would be made according to the two (2) isoforms of the D2 receptors. The D2/BR isoform directs towards a high carbohydrate consumption, without causing a gain in body weight. While D2/SUL, promotes high fat food consumption, causing an increase in body weight. In women, 17β-estradiol modulates the activity ratio between these two D2 receptor isoforms to ensure energy and homeostatic balance, stabilizing food intake and body weight.展开更多
Estrogen plays an important role in regulating Sertoli cell number in the testis.The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured,immature boar Sertoli cells via...Estrogen plays an important role in regulating Sertoli cell number in the testis.The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured,immature boar Sertoli cells via the estrogen receptor β(ERβ) and the cAMP-extracellular signal-regulated kinase(ERK1/2) pathway.Low levels(10-10-10-8 mol L-1) of 17β-estradiol increased cell number,but high levels(10-7-10-6 mol L-1) decreased it(P < 0.05).Sertoli cell number began to recover for an additional 24 h in the medium without 17β-estradiol(10-6 mol L-1)(P > 0.05).The effects of 17β-estradiol(10-9 mol L-1) peaked at the first 24 h(P < 0.05).17β-estradiol activated ERK1/2 from 5 min to 24 h,but the activiy of ERK1/2 began to decrease after 4 h.Both PD98059 and U0126,two ERK inhibitors,blocked cell division(P < 0.05).17β-estradiol(10-10-10-6 mol L-1) dose-dependently increased cAMP production(P < 0.05),and both 17β-estradiol(10-9 mol L-1) and forskolin,which increases cAMP levels,induced cell proliferation and activated ERK1/2(P < 0.05).Rp-cAMP,an antagonist of cAMP,blocked this 17β-estradiol activity(P < 0.05).Two estrogen receptor antagonists,ICI 182780 and ERβ antagonist(ERβAnt),reduced Sertoli cell number,cAMP production and ERK1/2 activation(P < 0.05),but ERαAnt did not(P > 0.05).Therefore,17βestradiol mainly promotes pig Sertoli cell proliferation via ERβ to induce cAMP production and ERK activation to promote cell proliferation.展开更多
Several epidemiological,cellular,and molecular studies demonstrate the role of environmental chemicals with endocrine disrupting activities,typical of Westernized societies,in the pathogenesis of numerous diseases inc...Several epidemiological,cellular,and molecular studies demonstrate the role of environmental chemicals with endocrine disrupting activities,typical of Westernized societies,in the pathogenesis of numerous diseases including cancer.Nonetheless this information,the design and execution of studies on endocrine disruptors are not yet cognizant that the specific actions of individual hormones often change with development and ageing,they may be different in males and females and may be mediated by different receptors isoforms expressed in different tissues or at different life stages.These statements are particularly true when assessing the hazard of endocrine disruptors against 17β-estradiol(E2)actions in that this hormone is crucial determinant of sexrelated differences in anatomical,physiological,and behavioral traits which characterize male and female physiology.Moreover,E2 is also involved in carcinogenesis.The oncogenic effects of E2 have been investigated extensively in breast and ovarian cancers where hormone-receptor modulators are now an integral part of targeted treatment.Little is known about the E2preventive signalling in colorectal cancer,although this disease is more common in men than women,the difference being more striking amongst pre-menopausal women and age-matched men.This review aims to dissect the role and action mechanisms of E2 in colorectal cancer evaluating the ability of estrogen disruptors(i.e.,xenoestrogens)in impair these E2 actions.Data discussed here lead to define the possible role of xenoestrogens in the impairment and/or activation of E2signals important for colorectal cancer prevention.展开更多
The aim of the present study was to investigate the long-term effects of 17β-estradiol(E2) exposure on gonadal development in the tiger puffer( Takifugu rubripe s), which has a genetic sex determination system of mal...The aim of the present study was to investigate the long-term effects of 17β-estradiol(E2) exposure on gonadal development in the tiger puffer( Takifugu rubripe s), which has a genetic sex determination system of male homogametic XY-XX. Tiger puffer larvae were exposed to 1, 10 and 100 μg/L E2 from 15 to 100 days post-hatch(dph) and then maintained in clean seawater until 400 dph. Changes in sex ratio, gonadal structure and gonadosomatic index(GSI) were monitored at 100, 160, 270 and 400 dph. Sex-associated single nucleotide polymorphism(SNP) markers were used to analyze the genetic sex of samples, except those at 100 dph. Exposure had a positive effect on the conversion of genetically male gonads into phenotypically female gonads at 100 dph. However, gonads from 60% of genetic XY males in the 1-μg/L E2 group and 100% in the 10-μg/L E2 group developed intersexual gonads at 160 dph; gonads of all genetic XY males in the two treatment groups reverted to testis by 270 dph. While 38%, 57% and 44% of gonads of XY fish in the 100-μg/L E2 group reverted to intersexual gonads at 160, 270 and 400 dph, respectively, none reverted to testis after E2 treatment. In addition, E2 exposure inhibited gonadal growth of both genetic sexes, as indicated by the clear dose-dependent decrease in GSI at 270 and 400 dph. The results showed that exposure to E2 during the early life stages of tiger puffer disrupted gonadal development, but that fish recovered after migration to clean seawater. The study suggests the potential use of tiger puffer as a valuable indicator species to evaluate the effects of environmental estrogens on marine fish, thereby protecting valuable fishery resources.展开更多
Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle.Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-estradiol (0.3, 3, 30 and 300 nmol/L) were ...Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle.Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-estradiol (0.3, 3, 30 and 300 nmol/L) were observed in vitro. The response of the muscle strips to estrogen after incubation with either actinomycin D (10μmol/L) or L-NAME (10μmol/L) were also evaluated. Inside-out mode of patch clamp in a single smooth muscle cell was applied to investigate the Maxi-K channel activities. Results: Estrogen caused a dose-dependent relaxation of the strips precontracted with norepinephrine. The maximal response was noted about 10 minutes after treatment. Theestrogen-induced relaxation was prevented by neither actinomycin D nor L-NAME, suggesting that the response was not mediated by gene transcription or nitric oxide (NO). Application of 17β-estradiol increased the Maxi-K channelactivities. Conclusion: 17β-estradiol may be involved in relaxation of rabbit cavernous smooth muscles via a nongenomic and NO independent mechanism. 17β-estradiol stimulates Maxi-K channel of the rabbit cavernous myocyte.展开更多
The efficacy of Endocrine Disrupting Compounds (EDCs), 17β-estradiol was tested on the fish Oreochromis niloticus in order to understand the intersex relationship of fish, in which sequential hermaphrodism can consis...The efficacy of Endocrine Disrupting Compounds (EDCs), 17β-estradiol was tested on the fish Oreochromis niloticus in order to understand the intersex relationship of fish, in which sequential hermaphrodism can consist of a male changing into a female (protandry) or a female changing into a male (protogyny). The fish were equally divided into 3 groups. The first group was the control group;the second and third groups were treated with 10 and 100 mg L-1 of 17β-estradiol, respectively, for 30 days. The overall result in this experiment had no significant effect on the growth parameters. Among the two treated groups, the low concentration group shows results similar to those of the control groups. The high concentration group shows changes to the male reproductive system with the appearance of the testis-ova present resulting in an intersex condition of the male gonads. With this experiment, it can be concluded that 17β-estradiol at high concentration reveals positive changes towards the male reproductive system of the fish, Oreochromis niloticus.展开更多
Background: Mechanisms underlying overeating-induced obesity in post-menopausal woman include functional lack of 17β-estradiol dysregulating dopamine D2 receptors, thereby inducing food addiction, glucose craving or ...Background: Mechanisms underlying overeating-induced obesity in post-menopausal woman include functional lack of 17β-estradiol dysregulating dopamine D2 receptors, thereby inducing food addiction, glucose craving or alcohol dependence through reward circuitry. This study aimed at further understanding 17β-estradiol and dopamine D2 receptors interferences in the etiology of woman obesity. Method: Seventy-two Wistar female rats weighing 200 - 205 g, individually-housed, were divided into non-ovariectomized control (C = 6 groups) and ovariectomized rats (OVX = 6 groups) which were concurrently subjected to the following treatments: Non-drug-treated (DMSO vehicle), 17β-estradiol (E2, 5 μg/kg, s.c.), sulpiride (SUL, 20 mg/kg, i.p.), bromocriptine (BR, 0.1 mg/kg, i.p.), E2 + SUL or E2 + BR, designating the 6 constitutive groups of either control or ovariectomy. Within each experimental group, consumption of different solutions (10% alcohol, 10% sucrose and water) as well as food intake and body weight were daily measured, for 10 consecutive days. Results: This study indicated that D2S was a specific inducer of alcohol and food intakes, but reduced sugar consumption. In addition, 17β- estradiol regulated the body weight set point, modulating D2S functions towards increased food intake at lower weights and decreased food intake at higher weights. D2S met the slow genomic actions induced by 17β-estradiol. Conversely, D2L inhibited alcohol and food intakes, but induced specifically sugar consumption, thereby regulating blood glucose levels and promoting energy expenditure in reducing body weight. Indeed, 17β-estradiol exerted a tonic inhibition on D2L which was released by OVX, exacerbating sugar intake and increasing body weight. D2L mediated the rapid metabolic effects of 17β-estradiol. Conclusion: Our results supported physiological data reporting that activation of the mostly expressed presynaptically D2S-class autoreceptors decreased dopamine release stimulating food intake, whereas activation of the predominantly postsynaptic isoform D2L receptors increased dopamine activity inhibiting food intake. Our studies indicated that 17β-estradiol acted on the two types of D2 receptors showing opposite functions to equilibrate energy intake vs. expenditure for weight set point regulation. Our data also supported biochemical findings reporting that 17β-estradiol induced D2 genes transcriptional regulation, thereby involving both types of D2 receptors in the etiology of obesity. The combined dysregulated effects of D2L and D2S receptors, as 17β-estradiol was lacking, would be causal factors underlying the etiology of obesity.展开更多
A highly-controllable core-shell silica-MIPs absorbent by anchoring a MIPs layer to the surface of SiO2 nanoparticles via a surface molecular imprinting process was prepared. The templates were covalently modified wit...A highly-controllable core-shell silica-MIPs absorbent by anchoring a MIPs layer to the surface of SiO2 nanoparticles via a surface molecular imprinting process was prepared. The templates were covalently modified with functional monomers to form precursor EstSi. The latter together with coupling reagent KH-570, were grafted onto the surface of SiO2 nanoparticles before polymerization, to ensure the quantity and quality of imprinted sites on the surface of the covalently attached matrix. The as-synthesized core-shell nanomaterials (SiO2@MIP2) were then evaluated for selective adsorption of 17β-estradiol (E2) with Raman spectra as detection method. The results indicate that SiO2@MIP2 can fast and selectively adsorb E2 from structural analogues, with detection limit of 0.01 μmol/l.展开更多
The phenomenon of sex dimorphism prevails among many fi sh species. It has attracted the general research interest due to its close relationship to fi sh growth and thus aquaculture productivity. In Chinese tongue sol...The phenomenon of sex dimorphism prevails among many fi sh species. It has attracted the general research interest due to its close relationship to fi sh growth and thus aquaculture productivity. In Chinese tongue sole ( Cynoglossus semilaevis ), 17β-estradiol (E2) can be used reportedly to induce the feminization of fi sh, although the detailed regulatory network remained elusive. We treated the tongue sole fry before sex diff erentiation with E2 (10 and 30 μg/L) to identify potential targets of E2 in Chinese tongue sole. The E2 treatment indeed induced genetic male fi sh sex-reversal to phenotypic female. Using an iTRAQ-based comparative proteomic analysis, 409 proteins that diff erentially expressed after E2 induction were identifi ed, including 259 up-regulated and 150 down-regulated proteins. Furthermore, 19 diff erentially expressed proteins identifi ed in the comparative proteomic analysis were selected to assess their transcription and eight of them exhibited the same tendency. Functions of the eight proteins included mainly nucleotide and protein binding. Interestingly, a far upstream element-binding protein 3-like isoform exhibited the signifi cant upregulation both at transcription and translation levels after E2 treatment. This work identifi ed a set of candidate proteins for E2 response and deepened our understanding of E2 regulatory mechanism.展开更多
Estrogen plays an important role in regulating testicular Sertoli cell number. Furthermore, S-phase kinase-associated protein 2(SKP2) plays a central role in mammalian cell cycle progression. The objective of this stu...Estrogen plays an important role in regulating testicular Sertoli cell number. Furthermore, S-phase kinase-associated protein 2(SKP2) plays a central role in mammalian cell cycle progression. The objective of this study was to determine whether 17β-estradiol can regulate the expression of SKP2, and the Sertoli cell cycle, via estrogen receptor β(ERβ), the cyclic adenosine monophosphate(cAMP)-protein kinase A(PKA) and extracellular signal-regulated kinase(ERK1/2) pathway. When cultured immature boar Sertoli cells were treated with 17β-estradiol, a time-dependent increase in SKP2 mRNA and protein level was observed by real-time PCR and Western blot, and 17β-estradiol activity peaked at 30 min. Tr eatment with ICI182780 and ERβ antagonist reduced 17β-estradiol-induced expression of SKP2 and proliferating cell nuclear antigen(PCNA), while increasing the protein concentration of p27kip1. However, the effect of ERα antagonist on these parameters was lower than that of ICI182780 and ERβ. Forskolin had a similar effect as 17β-estradiol on the expression of SKP2, PCNA and p27kip1. Rp-cAMP, H-89 and U0126 treatment reduced 17β-estradiol-induced changes, while H-89 also inhibited ERK1/2 activation. Therefore, 17β-estradiol mainly regulates SKP2 mRNA and protein expression via ERβ-cAMP-PKA and ERK1/2 activation. SKP2 and PCNA expression were positively correlated, while increased SKP2 expression likely resulted in p27kip1 degradation.展开更多
This study was conducted to assess the existing concentration of 17β-estradiol(E2)in the surface water samples collected from rivers and lakes around Klang Valley,Malaysia.E2,which is a natural feminizing chemical pr...This study was conducted to assess the existing concentration of 17β-estradiol(E2)in the surface water samples collected from rivers and lakes around Klang Valley,Malaysia.E2,which is a natural feminizing chemical produced in female organisms,regularly used to compare with other environmental estrogens because they behave similarly and react effectively as a hormone at a very low concentration.It was found that the average concentration of E2 in the aquatic environment of Klang Valley was(14.08 ±3.67)pg/mL,which was 14 times higher than those in the Japanese aquatic environment in this study.The river system had the average concentration of(20.02±5.26)pg/mL while the lake had an average concentration of(5.91±3.39)pg/mL.The E2 concentration was presumed high if the sources occurred nearby the area.Current levels of E2 in the aquatic environment may possess threats to existing aquatic organisms.Since high level of E2 has been discovered in the aquatic environment around Klang Valley,further studies and monitoring of E2 and other EDCs concentrations are needed to determine their levels in Malaysian aquatic environment and help to control these chemicals pollution in the aquatic environment.展开更多
Our previous studies showed that 17β-estradiol (E2) modulated dopamine D2 receptor in regulating body weight set-point. The aim of this study was to understand whether thiamine deficiency influenced the E2 modulation...Our previous studies showed that 17β-estradiol (E2) modulated dopamine D2 receptor in regulating body weight set-point. The aim of this study was to understand whether thiamine deficiency influenced the E2 modulation on dopamine D2 receptors, using bromocriptine mesylate (BR) and sulpiride (SUL) as selective central dopamine-D2 receptors agonist and antagonist respectively. We studied the E2-dopamine D2 receptors interferences in a 10-day thiamine-deficient female rats for which consumptions of water, sugar, alcohol and food were daily-recorded and their consequences on body weights assessed. Our results showed that the volume of water daily ingested doubled in thiamine-deficient female rats (OXT), while sugar and alcohol consumptions collapsed with decreased weight and food consumption. On the one hand, thiamine potentiated D2/BR activity (bromocriptine-activated D2 receptors) to induce sugar intake and inhibited the same D2/BR receptors to induce water intake. On the other hand, thiamine promoted D2/SUL receptors (sulpiride-inhibited D2 receptors) for enhanced alcohol intake, increased food consumption and weight gain. Taking together, thiamine modulated the actions of 17β-estradiol on both D2/BR and D2/SUL receptors activities.展开更多
The aim of this study was to compare serum 17β-estradiol of menopausal women with/without Oral Dryness (OD) feeling, and evaluate the re-lationship between serum 17β-estradiol and severity of OD feeling. A case-cont...The aim of this study was to compare serum 17β-estradiol of menopausal women with/without Oral Dryness (OD) feeling, and evaluate the re-lationship between serum 17β-estradiol and severity of OD feeling. A case-control study was carried out on 70 selected menopausal women aged 40 - 77 years with or without OD feeling (35 as case, 35 as control) conducted at the Clinic of Oral Medicine, Tehran University of Medical Sciences. Xerostomia inventory (XI) score was used as an index of OD feeling severity. The serum 17β-estradiol concentration was measured by an enzyme immunoassay kit (ELISA). Statistical analysis of Student’s t-test and Spearman correlation coefficient was used. The mean serum concentration of 17β-estradiol was significantly lower in case than control. There was a significant negative correlation between XI score and concentration of 17β-estradiol in menopausal women (r = –0.311, P = 0.004). It seems that there is a negatively slight correlation between OD feeling severity and serum 17β-estradiol in menopausal women.展开更多
文摘17β-estradiol modulates the activity of D2 receptors in the regulation of food intake and body weight. The functional lack of 17β-estradiol in postmenopausal women could create a dietary imbalance and cause body weight gain. This study aimed to better understand the interferences that could exist between 17β-estradiol, D2 receptors and the selection of carbohydrate, fat and protein consumption, as well as their consequences on body weight gain by using an animal model of the menopause. Ovariectomy exacerbates the consumption of foods rich in lipids. Thus confirming an inhibitory action of 17β-estradiol (E2) on the consumption of these types of foods. This consumption stimulates body weight gain, which is promoted by the high caloric content of these foods and not by the amount consumed. Our results showed a direct involvement of D2 receptors in food choice. This choice would be made according to the two (2) isoforms of the D2 receptors. The D2/BR isoform directs towards a high carbohydrate consumption, without causing a gain in body weight. While D2/SUL, promotes high fat food consumption, causing an increase in body weight. In women, 17β-estradiol modulates the activity ratio between these two D2 receptor isoforms to ensure energy and homeostatic balance, stabilizing food intake and body weight.
基金supported by the National Natural Science Foundation of China(30270955)the Foundamental Research Funds for the Central Universities,China(XDJK2009B035)
文摘Estrogen plays an important role in regulating Sertoli cell number in the testis.The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured,immature boar Sertoli cells via the estrogen receptor β(ERβ) and the cAMP-extracellular signal-regulated kinase(ERK1/2) pathway.Low levels(10-10-10-8 mol L-1) of 17β-estradiol increased cell number,but high levels(10-7-10-6 mol L-1) decreased it(P < 0.05).Sertoli cell number began to recover for an additional 24 h in the medium without 17β-estradiol(10-6 mol L-1)(P > 0.05).The effects of 17β-estradiol(10-9 mol L-1) peaked at the first 24 h(P < 0.05).17β-estradiol activated ERK1/2 from 5 min to 24 h,but the activiy of ERK1/2 began to decrease after 4 h.Both PD98059 and U0126,two ERK inhibitors,blocked cell division(P < 0.05).17β-estradiol(10-10-10-6 mol L-1) dose-dependently increased cAMP production(P < 0.05),and both 17β-estradiol(10-9 mol L-1) and forskolin,which increases cAMP levels,induced cell proliferation and activated ERK1/2(P < 0.05).Rp-cAMP,an antagonist of cAMP,blocked this 17β-estradiol activity(P < 0.05).Two estrogen receptor antagonists,ICI 182780 and ERβ antagonist(ERβAnt),reduced Sertoli cell number,cAMP production and ERK1/2 activation(P < 0.05),but ERαAnt did not(P > 0.05).Therefore,17βestradiol mainly promotes pig Sertoli cell proliferation via ERβ to induce cAMP production and ERK activation to promote cell proliferation.
基金Acknowledgment This work was supported by the National Natural Science Foundation of China （No. 30200195）. We thank Dr Hai-Bin Wang for taking photographs and Dr Su-Hui Wu （Henan Normal University, China） for statistical analysis. We thank the faculty of Huanghuai University for supporting Dr En-Zhong Li.
文摘Several epidemiological,cellular,and molecular studies demonstrate the role of environmental chemicals with endocrine disrupting activities,typical of Westernized societies,in the pathogenesis of numerous diseases including cancer.Nonetheless this information,the design and execution of studies on endocrine disruptors are not yet cognizant that the specific actions of individual hormones often change with development and ageing,they may be different in males and females and may be mediated by different receptors isoforms expressed in different tissues or at different life stages.These statements are particularly true when assessing the hazard of endocrine disruptors against 17β-estradiol(E2)actions in that this hormone is crucial determinant of sexrelated differences in anatomical,physiological,and behavioral traits which characterize male and female physiology.Moreover,E2 is also involved in carcinogenesis.The oncogenic effects of E2 have been investigated extensively in breast and ovarian cancers where hormone-receptor modulators are now an integral part of targeted treatment.Little is known about the E2preventive signalling in colorectal cancer,although this disease is more common in men than women,the difference being more striking amongst pre-menopausal women and age-matched men.This review aims to dissect the role and action mechanisms of E2 in colorectal cancer evaluating the ability of estrogen disruptors(i.e.,xenoestrogens)in impair these E2 actions.Data discussed here lead to define the possible role of xenoestrogens in the impairment and/or activation of E2signals important for colorectal cancer prevention.
基金Supported by the China Agriculture Research System(No.CARS-50-G20)the National Natural Science Foundation of China(No.31402284)the National High Technology Research and Development Program of China(863 Program)(No.2012AA10A413-2)
文摘The aim of the present study was to investigate the long-term effects of 17β-estradiol(E2) exposure on gonadal development in the tiger puffer( Takifugu rubripe s), which has a genetic sex determination system of male homogametic XY-XX. Tiger puffer larvae were exposed to 1, 10 and 100 μg/L E2 from 15 to 100 days post-hatch(dph) and then maintained in clean seawater until 400 dph. Changes in sex ratio, gonadal structure and gonadosomatic index(GSI) were monitored at 100, 160, 270 and 400 dph. Sex-associated single nucleotide polymorphism(SNP) markers were used to analyze the genetic sex of samples, except those at 100 dph. Exposure had a positive effect on the conversion of genetically male gonads into phenotypically female gonads at 100 dph. However, gonads from 60% of genetic XY males in the 1-μg/L E2 group and 100% in the 10-μg/L E2 group developed intersexual gonads at 160 dph; gonads of all genetic XY males in the two treatment groups reverted to testis by 270 dph. While 38%, 57% and 44% of gonads of XY fish in the 100-μg/L E2 group reverted to intersexual gonads at 160, 270 and 400 dph, respectively, none reverted to testis after E2 treatment. In addition, E2 exposure inhibited gonadal growth of both genetic sexes, as indicated by the clear dose-dependent decrease in GSI at 270 and 400 dph. The results showed that exposure to E2 during the early life stages of tiger puffer disrupted gonadal development, but that fish recovered after migration to clean seawater. The study suggests the potential use of tiger puffer as a valuable indicator species to evaluate the effects of environmental estrogens on marine fish, thereby protecting valuable fishery resources.
文摘Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle.Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-estradiol (0.3, 3, 30 and 300 nmol/L) were observed in vitro. The response of the muscle strips to estrogen after incubation with either actinomycin D (10μmol/L) or L-NAME (10μmol/L) were also evaluated. Inside-out mode of patch clamp in a single smooth muscle cell was applied to investigate the Maxi-K channel activities. Results: Estrogen caused a dose-dependent relaxation of the strips precontracted with norepinephrine. The maximal response was noted about 10 minutes after treatment. Theestrogen-induced relaxation was prevented by neither actinomycin D nor L-NAME, suggesting that the response was not mediated by gene transcription or nitric oxide (NO). Application of 17β-estradiol increased the Maxi-K channelactivities. Conclusion: 17β-estradiol may be involved in relaxation of rabbit cavernous smooth muscles via a nongenomic and NO independent mechanism. 17β-estradiol stimulates Maxi-K channel of the rabbit cavernous myocyte.
文摘The efficacy of Endocrine Disrupting Compounds (EDCs), 17β-estradiol was tested on the fish Oreochromis niloticus in order to understand the intersex relationship of fish, in which sequential hermaphrodism can consist of a male changing into a female (protandry) or a female changing into a male (protogyny). The fish were equally divided into 3 groups. The first group was the control group;the second and third groups were treated with 10 and 100 mg L-1 of 17β-estradiol, respectively, for 30 days. The overall result in this experiment had no significant effect on the growth parameters. Among the two treated groups, the low concentration group shows results similar to those of the control groups. The high concentration group shows changes to the male reproductive system with the appearance of the testis-ova present resulting in an intersex condition of the male gonads. With this experiment, it can be concluded that 17β-estradiol at high concentration reveals positive changes towards the male reproductive system of the fish, Oreochromis niloticus.
文摘Background: Mechanisms underlying overeating-induced obesity in post-menopausal woman include functional lack of 17β-estradiol dysregulating dopamine D2 receptors, thereby inducing food addiction, glucose craving or alcohol dependence through reward circuitry. This study aimed at further understanding 17β-estradiol and dopamine D2 receptors interferences in the etiology of woman obesity. Method: Seventy-two Wistar female rats weighing 200 - 205 g, individually-housed, were divided into non-ovariectomized control (C = 6 groups) and ovariectomized rats (OVX = 6 groups) which were concurrently subjected to the following treatments: Non-drug-treated (DMSO vehicle), 17β-estradiol (E2, 5 μg/kg, s.c.), sulpiride (SUL, 20 mg/kg, i.p.), bromocriptine (BR, 0.1 mg/kg, i.p.), E2 + SUL or E2 + BR, designating the 6 constitutive groups of either control or ovariectomy. Within each experimental group, consumption of different solutions (10% alcohol, 10% sucrose and water) as well as food intake and body weight were daily measured, for 10 consecutive days. Results: This study indicated that D2S was a specific inducer of alcohol and food intakes, but reduced sugar consumption. In addition, 17β- estradiol regulated the body weight set point, modulating D2S functions towards increased food intake at lower weights and decreased food intake at higher weights. D2S met the slow genomic actions induced by 17β-estradiol. Conversely, D2L inhibited alcohol and food intakes, but induced specifically sugar consumption, thereby regulating blood glucose levels and promoting energy expenditure in reducing body weight. Indeed, 17β-estradiol exerted a tonic inhibition on D2L which was released by OVX, exacerbating sugar intake and increasing body weight. D2L mediated the rapid metabolic effects of 17β-estradiol. Conclusion: Our results supported physiological data reporting that activation of the mostly expressed presynaptically D2S-class autoreceptors decreased dopamine release stimulating food intake, whereas activation of the predominantly postsynaptic isoform D2L receptors increased dopamine activity inhibiting food intake. Our studies indicated that 17β-estradiol acted on the two types of D2 receptors showing opposite functions to equilibrate energy intake vs. expenditure for weight set point regulation. Our data also supported biochemical findings reporting that 17β-estradiol induced D2 genes transcriptional regulation, thereby involving both types of D2 receptors in the etiology of obesity. The combined dysregulated effects of D2L and D2S receptors, as 17β-estradiol was lacking, would be causal factors underlying the etiology of obesity.
文摘A highly-controllable core-shell silica-MIPs absorbent by anchoring a MIPs layer to the surface of SiO2 nanoparticles via a surface molecular imprinting process was prepared. The templates were covalently modified with functional monomers to form precursor EstSi. The latter together with coupling reagent KH-570, were grafted onto the surface of SiO2 nanoparticles before polymerization, to ensure the quantity and quality of imprinted sites on the surface of the covalently attached matrix. The as-synthesized core-shell nanomaterials (SiO2@MIP2) were then evaluated for selective adsorption of 17β-estradiol (E2) with Raman spectra as detection method. The results indicate that SiO2@MIP2 can fast and selectively adsorb E2 from structural analogues, with detection limit of 0.01 μmol/l.
基金Supported by the Natural Science Foundation of Shandong Province(No.ZR2014CQ053)the National Natural Science Foundation of China(No.31402293)the Taishan Scholar Climbing Program of Shandong Province,China
文摘The phenomenon of sex dimorphism prevails among many fi sh species. It has attracted the general research interest due to its close relationship to fi sh growth and thus aquaculture productivity. In Chinese tongue sole ( Cynoglossus semilaevis ), 17β-estradiol (E2) can be used reportedly to induce the feminization of fi sh, although the detailed regulatory network remained elusive. We treated the tongue sole fry before sex diff erentiation with E2 (10 and 30 μg/L) to identify potential targets of E2 in Chinese tongue sole. The E2 treatment indeed induced genetic male fi sh sex-reversal to phenotypic female. Using an iTRAQ-based comparative proteomic analysis, 409 proteins that diff erentially expressed after E2 induction were identifi ed, including 259 up-regulated and 150 down-regulated proteins. Furthermore, 19 diff erentially expressed proteins identifi ed in the comparative proteomic analysis were selected to assess their transcription and eight of them exhibited the same tendency. Functions of the eight proteins included mainly nucleotide and protein binding. Interestingly, a far upstream element-binding protein 3-like isoform exhibited the signifi cant upregulation both at transcription and translation levels after E2 treatment. This work identifi ed a set of candidate proteins for E2 response and deepened our understanding of E2 regulatory mechanism.
基金grants from the National Natural Science Foundation of China(31072183)the Fundamental Research Funds for the Central Universities,China(XDJK2009B035)
文摘Estrogen plays an important role in regulating testicular Sertoli cell number. Furthermore, S-phase kinase-associated protein 2(SKP2) plays a central role in mammalian cell cycle progression. The objective of this study was to determine whether 17β-estradiol can regulate the expression of SKP2, and the Sertoli cell cycle, via estrogen receptor β(ERβ), the cyclic adenosine monophosphate(cAMP)-protein kinase A(PKA) and extracellular signal-regulated kinase(ERK1/2) pathway. When cultured immature boar Sertoli cells were treated with 17β-estradiol, a time-dependent increase in SKP2 mRNA and protein level was observed by real-time PCR and Western blot, and 17β-estradiol activity peaked at 30 min. Tr eatment with ICI182780 and ERβ antagonist reduced 17β-estradiol-induced expression of SKP2 and proliferating cell nuclear antigen(PCNA), while increasing the protein concentration of p27kip1. However, the effect of ERα antagonist on these parameters was lower than that of ICI182780 and ERβ. Forskolin had a similar effect as 17β-estradiol on the expression of SKP2, PCNA and p27kip1. Rp-cAMP, H-89 and U0126 treatment reduced 17β-estradiol-induced changes, while H-89 also inhibited ERK1/2 activation. Therefore, 17β-estradiol mainly regulates SKP2 mRNA and protein expression via ERβ-cAMP-PKA and ERK1/2 activation. SKP2 and PCNA expression were positively correlated, while increased SKP2 expression likely resulted in p27kip1 degradation.
文摘This study was conducted to assess the existing concentration of 17β-estradiol(E2)in the surface water samples collected from rivers and lakes around Klang Valley,Malaysia.E2,which is a natural feminizing chemical produced in female organisms,regularly used to compare with other environmental estrogens because they behave similarly and react effectively as a hormone at a very low concentration.It was found that the average concentration of E2 in the aquatic environment of Klang Valley was(14.08 ±3.67)pg/mL,which was 14 times higher than those in the Japanese aquatic environment in this study.The river system had the average concentration of(20.02±5.26)pg/mL while the lake had an average concentration of(5.91±3.39)pg/mL.The E2 concentration was presumed high if the sources occurred nearby the area.Current levels of E2 in the aquatic environment may possess threats to existing aquatic organisms.Since high level of E2 has been discovered in the aquatic environment around Klang Valley,further studies and monitoring of E2 and other EDCs concentrations are needed to determine their levels in Malaysian aquatic environment and help to control these chemicals pollution in the aquatic environment.
文摘Our previous studies showed that 17β-estradiol (E2) modulated dopamine D2 receptor in regulating body weight set-point. The aim of this study was to understand whether thiamine deficiency influenced the E2 modulation on dopamine D2 receptors, using bromocriptine mesylate (BR) and sulpiride (SUL) as selective central dopamine-D2 receptors agonist and antagonist respectively. We studied the E2-dopamine D2 receptors interferences in a 10-day thiamine-deficient female rats for which consumptions of water, sugar, alcohol and food were daily-recorded and their consequences on body weights assessed. Our results showed that the volume of water daily ingested doubled in thiamine-deficient female rats (OXT), while sugar and alcohol consumptions collapsed with decreased weight and food consumption. On the one hand, thiamine potentiated D2/BR activity (bromocriptine-activated D2 receptors) to induce sugar intake and inhibited the same D2/BR receptors to induce water intake. On the other hand, thiamine promoted D2/SUL receptors (sulpiride-inhibited D2 receptors) for enhanced alcohol intake, increased food consumption and weight gain. Taking together, thiamine modulated the actions of 17β-estradiol on both D2/BR and D2/SUL receptors activities.
文摘The aim of this study was to compare serum 17β-estradiol of menopausal women with/without Oral Dryness (OD) feeling, and evaluate the re-lationship between serum 17β-estradiol and severity of OD feeling. A case-control study was carried out on 70 selected menopausal women aged 40 - 77 years with or without OD feeling (35 as case, 35 as control) conducted at the Clinic of Oral Medicine, Tehran University of Medical Sciences. Xerostomia inventory (XI) score was used as an index of OD feeling severity. The serum 17β-estradiol concentration was measured by an enzyme immunoassay kit (ELISA). Statistical analysis of Student’s t-test and Spearman correlation coefficient was used. The mean serum concentration of 17β-estradiol was significantly lower in case than control. There was a significant negative correlation between XI score and concentration of 17β-estradiol in menopausal women (r = –0.311, P = 0.004). It seems that there is a negatively slight correlation between OD feeling severity and serum 17β-estradiol in menopausal women.
