scholarly journals Modulation of appetite by gonadal steroid hormones

2006 ◽  
Vol 361 (1471) ◽  
pp. 1251-1263 ◽  
Author(s):  
Lori Asarian ◽  
Nori Geary
Keyword(s):  
Sex Differences ◽  
Food Intake ◽  
Steroid Hormones ◽  
Nucleus Tractus Solitarius ◽  
Female Rats ◽  
Gonadal Steroid Hormones ◽  
Gonadal Steroid ◽  
Feedback Controls ◽  
Cyclic Changes ◽  
Rats And Mice

Several sex differences in eating, their control by gonadal steroid hormones and their peripheral and central mediating mechanisms are reviewed. Adult female rats and mice as well as women eat less during the peri-ovulatory phase of the ovarian cycle (estrus in rats and mice) than other phases, an effect under the control of cyclic changes in estradiol secretion. Women also appear to eat more sweets during the luteal phase of the cycle than other phases, possibly due to simultaneous increases in estradiol and progesterone. In rats and mice, gonadectomy reveals further sex differences: orchiectomy decreases food intake by decreasing meal frequency and ovariectomy increases food intake by increasing meal size. These changes are reversed by testosterone and estradiol treatment, respectively. A variety of peripheral feedback controls of eating, including ghrelin, cholecystokinin (CCK), glucagon, hepatic fatty acid oxidation, insulin and leptin, has been shown to be estradiol-sensitive under at least some conditions and may mediate the estrogenic inhibition of eating. Of these, most progress has been made in the case of CCK. Neurons expressing estrogen receptor-α in the nucleus tractus solitarius of the brainstem appear to increase their sensitivity to CCK-induced vagal afferent input so as to lead to an increase in the satiating potency of CCK, and consequently decreased food intake, during the peri-ovulatory period in rats. Central serotonergic mechanisms also appear to be part of the effect of estradiol on eating. The physiological roles of other peripheral feedback controls of eating and their central mediators remain to be established.

Sex Differences in Sepsis Survival Involve Effects of Gonadal Steroid Hormones

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Sanjukta Chakraborty ◽  
Lavanya Venkatasamy ◽  
John N. Stallone
Keyword(s):  
Sex Differences ◽  
Steroid Hormones ◽  
Gonadal Steroid Hormones ◽  
Gonadal Steroid ◽  
Sepsis Survival

Neonatal gonadal hormones and blood pressure in the spontaneously hypertensive rat

1984 ◽  
Vol 247 (2) ◽  
pp. E258-E264 ◽  
Author(s):  
L. J. Cambotti ◽  
F. E. Cole ◽  
A. A. Gerall ◽  
E. D. Frohlich ◽  
A. A. MacPhee
Keyword(s):  
Blood Pressure ◽  
Steroid Hormones ◽  
Spontaneously Hypertensive Rat ◽  
Gonadal Hormones ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Gonadal Steroid Hormones ◽  
Gonadal Steroid ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

In rats, gonadal steroid hormones present during the neonatal period produce permanent or "organizational" effects that play a role in the sexual differentiation of the brain and sexually dimorphic patterns of behavior. Because there exists a sexually dimorphic pattern in the development of hypertension in the spontaneously hypertensive rat (SHR), we examined the influence of neonatal gonadal hormones on arterial pressure and body weight in these rats. Male SHR rats were castrated or sham-operated (controls) on their day of birth. Female rats received 1.25 mg testosterone propionate (TP) or sesame oil vehicle on their 2nd day of life. Sham-operated males and TP and oil females were gonadectomized at 81 days of age. To examine the transient or "activational" effects of gonadal steroid hormones, testosterone implants were placed subcutaneously in all rats at 128 days of age and were removed at 170 days of age. The rats were killed at 202 days of age, and selected organ weights were determined. During the original treatment, days 44-79, blood pressure in castrated males was comparable to that of control females, whereas blood pressure in neonatal TP females was not different from that of control males. When exposed to testosterone in adulthood, blood pressure increased more in neonatal TP female rats than in control females. Partial correlation analysis indicated that differences in body weights among the groups could not account for their variances in blood pressure. These data suggest that the neonatal gonadal hormone milieu contributes significantly to the sexually dimorphic pattern of hypertension development in the SHR.

129 UTERINE EXPRESSION OF TRANSIENT RECEPTOR POTENTIAL MELASTATIN 2 CHANNEL AND ITS REGULATION BY SEX STEROID HORMONES

2014 ◽  
Vol 26 (1) ◽  
pp. 178
Author(s):  
C. Ahn ◽  
E. J. Hong ◽  
E. B. Jeung
Keyword(s):  
Steroid Hormones ◽  
Mammalian Cells ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Independent Effect ◽  
Gonadal Steroid Hormones ◽  
Gonadal Steroid ◽  
Transient Receptor Potential Melastatin

The transient potential receptor (TRP) channels are membrane-binding proteins that are non-selectively permeable for cations, such as Ca2+ and Mg2+, in numerous mammalian cells. The extracellular or intracellular ions play key roles in physiological function, including muscle contraction, cytokine production, insulin release, and apoptosis. Although TRPM channels have been implicated in the brain, bone marrow, and spleen, the presence of TRPM2 has been reported in the endometrium of the uterus. To determine whether expression of the TRPM2 gene in the uterus is due to gonadal steroid hormones or a hormone-independent effect, the uterine TRPM2 gene was monitored in mature rats during the oestrous cycle and in immature rats after treatment with gonadal steroid oestrogen (E2), progesterone (P4) with/without their antagonist, ICI 182,780, and RU486. Dramatic induction of the level of TRPM2 mRNA occurs at proestrus, followed by a drop to baseline levels at metestrus, and its level is restored at diestrus. Furthermore, the immune-reactive TRPM2 is observed in stromal cells of the myometrium and endometrium, and changes during the oestrus cycle. In addition, E2-induced TRPM2 is inhibited by co-treatment with P4. Taken together, these results imply that TRPM2 expression levels in the uterus are regulated by gonadal steroid hormones E2 and P4. Results of this study suggest possible involvement of TRPM2 in reproductive function during the oestrous cycle in female rats.

scholarly journals Impact of sex in the prevalence and progression of glioblastomas: the role of gonadal steroid hormones

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Claudia Bello-Alvarez ◽  
Ignacio Camacho-Arroyo
Keyword(s):  
Cell Proliferation ◽  
Steroid Hormones ◽  
Physiological State ◽  
Migration And Invasion ◽  
Low Grade ◽  
Main Body ◽  
Protective Effects ◽  
Gonadal Steroid Hormones ◽  
Gonadal Steroid

Abstract Background As in other types of cancers, sex is an essential factor in the origin and progression of glioblastomas. Research in the field of endocrinology and cancer suggests that gonadal steroid hormones play an important role in the progression and prevalence of glioblastomas. In the present review, we aim to discuss the actions and mechanism triggered by gonadal steroid hormones in glioblastomas. Main body Glioblastoma is the most common malignant primary brain tumor. According to the epidemiological data, glioblastomas are more frequent in men than in women in a 1.6/1 proportion both in children and adults. This evidence, and the knowledge about sex influence over the prevalence of countless diseases, suggest that male gonadal steroid hormones, such as testosterone, promote glioblastomas growth. In contrast, a protective role of female gonadal steroid hormones (estradiol and progesterone) against glioblastomas has been questioned. Several pieces of evidence demonstrate a variety of effects induced by female and male gonadal steroid hormones in glioblastomas. Several studies indicate that pregnancy, a physiological state with the highest progesterone and estradiol levels, accelerates the progression of low-grade astrocytomas to glioblastomas and increases the symptoms associated with these tumors. In vitro studies have demonstrated that progesterone has a dual role in glioblastoma cells: physiological concentrations promote cell proliferation, migration, and invasion while very high doses (out physiological range) reduce cell proliferation and increases cell death. Conclusion Gonadal steroid hormones can stimulate the progression of glioblastomas through the increase in proliferation, migration, and invasion. However, the effects mentioned above depend on the concentrations of these hormones and the receptor involved in hormone actions. Estradiol and progesterone can exert promoter or protective effects while the role of testosterone has been always associated to glioblastomas progression.

scholarly journals Androgen sulphate formation in male and female mice

1969 ◽  
Vol 115 (3) ◽  
pp. 489-493
Author(s):  
D A Lewis
Keyword(s):  
Sex Differences ◽  
Sulphuric Acid ◽  
Female Rats ◽  
Dehydroepiandrosterone Sulphate ◽  
Male And Female ◽  
Female Mice ◽  
Liver Slices ◽  
Rats And Mice

1. After the administration of large doses of androsterone, epiandrosterone, dehydroepiandrosterone and testosterone to mice, females excreted more of the dose conjugated with sulphuric acid than did males. 2. Liver slices from female mice conjugated androgens with sulphuric acid to a greater extent than did slices from males. 3. Sulphotransferase preparations from livers of female rats and mice catalysed the formation of dehydroepiandrosterone sulphate at a faster rate than preparations from livers of the male animals. 4. A possible explanation for the observed sex differences is discussed.

scholarly journals Similar levels of emotional contagion in male and female rats

2019 ◽  
Author(s):  
Yingying Han ◽  
Bo Sichterman ◽  
Maria Carrillo ◽  
Valeria Gazzola ◽  
Christian Keysers
Keyword(s):  
Sex Differences ◽  
Social Life ◽  
Emotional Contagion ◽  
Female Rats ◽  
Male Rats ◽  
Neural Basis ◽  
Male And Female Rats ◽  
Danger Detection ◽  
Rats And Mice ◽  
Shed Light

AbstractEmotional contagion, the ability to feel what other individuals feel, is thought to be an important element of social life. In humans, emotional contagion has been shown to be stronger in women than men. Emotional contagion has been shown to exist also in rodents, and a growing number of studies explore the neural basis of emotional contagion in male rats and mice. These studies promise to shed light on the mechanisms that might go astray in psychiatric disorders characterized by dysfunctions of emotional contagion and empathy. Here we explore whether there are sex differences in emotional contagion in rats. We use an established paradigm in which a demonstrator rat receives footshocks while freezing is measured in both the demonstrator and an observer rat, which can hear, smell and see each other. By comparing pairs of male rats with pairs of female rats, we find (i) that female demonstrators freeze less when submitted to footshocks, but that (ii) the emotional contagion response, i.e. the degree of influence across the rats, does not depend on the sex of the rats. This was true whether emotional contagion was quantified based on the slope of a regression linking demonstrator and observer average freezing, or on Granger causality estimates of moment-to-moment freezing. The lack of sex differences in emotional contagion is compatible with an interpretation of emotional contagion as serving selfish danger detection.

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