Although the inﬂuence of sex on sleep pattern and cardiovascular parameters is well known, knowledge re- garding the effects of sleep loss on heart responses in both sexes is scarce. The present study investigated the effects of paradoxical sleep deprivation (PSD) and chronic sleep restriction (SR) on cardiovascular parame- ters and adrenocorticotropichormone (ACTH) levels in male and female rats. Both groups were randomly assigned to PSD for 96 h, SR for 21 days or home-cage control. Mean arterial pressure (MAP), heart rate (HR), baroreﬂex sensitivity (bradycardia and tachycardia responses) and ACTH levels were evaluated. The results showed that PSD induced a signiﬁcant increase in HR and ACTH levels in both sexes, although male rats presented higher levels of ACTH hormone compared to females. In addition to sex-speciﬁc responses, PSD decreased the tachycardia only in male rats. SR, induced a signiﬁcant increase in MAP and decrease in bradycardia in both sexes. Male rats were more affected by sleep deprivation protocols than females for MAP, bradycardia response, and ACTH levels. The results showed that the effects of sleep loss on cardiovascular parameters are associated with the protocol of sleep deprivation and that sex can modulate these effects. We suggested this experimental model as a suitable tool for further investigations of the relationship between cardiovascular parameters and sleep.
The existence of a circadian rhythm of atrial natriuretic peptide (ANP) in humans is controversial. We studied the plasma ANP response to isotonic blood volume expansion in the morning and in the afternoon and its relationship with adrenocorticotropichormone (ACTH)-corti- sol diurnal variation in seven normal subjects. Basal plasma ANP level was similar in the morning (19.6 ± 2.4 pg/ml) and in the afternoon (21.8 ± 4.8 pg/ml). The ANP peak obtained with saline infusion (0.9% NaCl, 12 ml/kg) in the morning (49.4 ± 8 pg/ml) did not differ from that obtained in the afternoon (60.3 ± 10.1 pg/ml). There was no correlation between the individual mean cortisol and ACTH levels and the ANP peak obtained with saline infusion. These data indicate no diurnal variation in plasma ANP secretion induced by blood volume expansion and no relationship between plasma ANP peak and ACTH-cortisol diurnal variation.
Figure 2. Plasma hormone levels: prolactin (Prl), luteinizing hormone (LH), corticosterone (CT), and adrenocorticotropichormone (ACTH) in the following groups: I, no manipulation; II, 30 min for adaptation of the animals of the same original group to a new cage; III, 30 min for adaptation of the animal isolated from the group and placed in a new cage; IV, 30 min for adaptation and 15 min for the collective exploratory test; V, 30 min for adaptation and 15 min for the individual exploratory test. For plasma ACTH determination, the groups were divided into two subgroups: “S” (the most stressed animal in the cage) and “P” (the other two partners). *P < 0.05, significant differences were observed between a) group I vs II, b) group I vs III, c) group I vs IV, d) group I vs V, e) group III vs V (one-way ANOVA). + P < 0.05, significant differences were observed between subgroups “S” and “P” within each experimental group for ACTH. The number of animals was 17 for the determination of CT, 17-18 for LH, and 15-17 for Prl. For ACTH, the number of animals was 6/12 for subgroups “S” and “P” in groups I and II, 6/9 for group III, 6/10 for group IV, and 6/11 for group V.
Allgrove (Triple A) syndrome is a rare autosomal recessive disorder characterized by cardinal features of adrenal insufficiency due to adrenocorticotropichormone (ACTH) resistance, achalasia, and alacrimia. It is frequently associated with neurological manifestations like polyneuropathy. Since its first description by Allgrove in 1978, approximately 100 cases have been reported in the literature. Here we report an 18-year-old boy diagnosed as having Allgrove syndrome, with ACTH resistant adrenal insuf- ficiency, achalasia, alacrimia, and severe motor polyneuropathy. Alacrimia was the earliest feature evident at the age of 8 years. He presented with achalasia and adrenal insufficiency at 12 and 18 years respectively and developed neurological symptoms in the form of severe muscle wasting at the age of 15 years. Patients with Allgrove syndrome usually manifest adrenal insufficiency and achalasia during first decade of life. Our patient manifested adrenal insufficiency and achalasia in the second decade and manifested neurological dysfunction before adrenal dysfunction.
RESULTS: The endocrine assessment was made at a mean of 7.4 days (standard deviation ¡6.6) after subarachnoid hemorrhage. Forty-four (66.7%) female and 22 (33.3%) male patients were evaluated. Thirty-nine patients (59.1%) had some type of pituitary dysfunction. Follicle-stimulating hormone/luteinizing hormone deficiency was the most frequent disorder (34.8%), followed by growth hormone/insulin growth factor (28.7%), adrenocorticotropichormone (18.1%) and thyroid-stimulating hormone (9%). Seventeen (25.7%) patients showed deficiencies in more than one axis. A greater incidence of hormone deficiency was observed in patients with a Glasgow Coma Scale score #13 (t test, p = 0.008), Hunt-Hess grade $4 (t test, p,0.001), or Fisher grade 4 (t test, p = 0.039). Hormone deficiency was not significantly associated (p.0.05) with increased hospitalization or clinical outcome.
Tibetan (TB) and Bama (BM) miniature pigs are two popular pig breeds that are used as experimental animals in China due to their small body size. Here, we analyzed single-nucleotide polymorphisms (SNPs) in gene fragments that are closely related to growth traits [growth hormone (GH), growth hormone receptor (GHR), and insulin-like growth factor (IGF)-1)] in these pig breeds and a large white (LW) control pig breed. On the basis of the analysis of 100 BMs, 108 TBs, and 50 LWs, the polymorphic distribution levels of GH, GHR, and IGF-1 were significantly different among these three pig breeds. According to correlation analyses between SNPs and five growth traits – – body weight (BW), body length (BL), withers height (WH), chest circumference (CC), and abdomen circumference (AC) – – three SNP loci in BMs and four SNP loci in TBs significantly affected growth traits. Three SNP sites in BMs and four SNP sites in TBs significantly affected growth traits. SNPs located in the GH gene fragment significantly affected BL and CC at locus 12 and BL at locus 45 in BMs, and also BW, WH, CC, and AC at locus 45 and WH and CC at locus 93 in TBs. One SNP at locus 85 in the BM GHR gene fragment significantly affected all growth traits. All indices were significantly reduced with a mixture of alleles at locus 85. These results provide more information regarding the genetic background of these minipig species and indicate useful selection markers for pig breeding programs.
Gonadotropin-releasing hormone (GnRH) is a hypothalamic decapeptide that stimulates gonadotropes in the anterior pituitary gland to release gonadotropins, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) by binding to the type I GnRH receptor (GnRHR), a speciﬁc G protein-coupled receptor (Sealfon et al., 1997). In the ovary, GnRH accumulates in the median eminence before ovulation. The release of GnRH is controlled by the nervous nuclei of the hypothalamus and the levels of estrogen and progesterone, which are produced by the
Growth hormone-releasing hormone (GHRH) and somatostatin modulate growth hormone (GH) secretion. A third mechanism was discovered in the last decade, involving the action of growth hormone secretagogues (GHS). Ghrelin, the endogenous ligand of the GHS-receptor, is an acylated peptide mainly produced by the stomach, but also synthesized in the hypothalamus. This compound increases both GH release and food intake. Endogenous ghrelin might amplify the basic pattern of GH secretion, optimizing soma- totroph responsiveness to GHRH, activating multiple interdependent intracel- lular pathways. However, its main site of action is the hypothalamus. In the current paper it is reviewed the available data on the discovery of this pep- tide, the mechanisms of action and possible physiological roles of the GHS and ghrelin on GH secretion, and finally, the possible therapeutic applications of these compounds. (Arq Bras Endocrinol Metab 2008; 52/5:726-733)
Em 1977, antes da descoberta do GH RH , Bow- ers e cols. desenvolveram pequenos peptídeos sintéti- cos, que eram capazes de liberar GH , a partir da molécula de met-encefalina (2). Posteriormente, esta descoberta levou à síntese de um novo hexapeptídeo, denominado de GH RP-6 (growth hormone releasing peptide) (3). Este peptídeo promove a liberação de GH por mecanismos não totalmente esclarecidos, porém diferentes dos utilizados pelo GH RH (4). Estudos realizados com estes secretagogos de GH (GH S) nesta ultima década vieram reforçar a hipótese de existir um papel fisiológico destes compostos na regulação da secreção de GH (5). A presença de receptores específi- cos para o GH RP, tanto no hipotálamo quanto na hipófise, apontava para a existência de um peptídeo endógeno semelhante, que, porém, ainda não havia sido identificado (6,7). A clonagem do receptor “órfão” dos GH S, em 1996, veio comprovar a hipótese da existência deste sistema de controle da secreção de GH (8). Este receptor pertence ao grupo de receptores ligados à proteína G, sendo expresso na hipófise anteri- or, hipotálamo e outras áreas do SNC. Finalmente, em 1999, Kojima e col. clonaram o ligante endógeno dos GH S, que foi isolado no estômago, e denominado de ghrelina (9). A estrutura deste peptídeo, que é acilado, é completamente diferente dos peptídeos conhecidos, e também da estrutura química dos GH S (10). A modi- ficação n-octanoil do resíduo serina na posição 3 da molécula é fundamental para a atividade biológica do peptídeo (9). A ghrelina promove a liberação de GH tanto in vivo quanto in vitro, em animais e no homem, de modo dose dependente (9,11). Estudos no homem mostram que a administração de ghrelina é capaz de liberar GH de modo potente, sendo muito maior seu efeito que o do GH RH , em doses equimolares (12). A descoberta da ghrelina veio comprovar a existência de uma terceira via de regulação da secreção de GH . Entretanto, não se conhece ainda o papel desta via na fisiologia e fisiopatologia da secreção de GH .
This study focuses on the construction of male hormonal decline relating to aging as part of a more general process of medicalization of male sexuality and aging. In order to accomplish this objective, 14 websites of pharmaceutical laboratories that sell drugs for male sexual health and seven websites of medical-scientific associations focusing on male sexual health were surveyed. We used the images found on these sites as analysis material. Based on our analysis, we discuss the existence of a partnership between the medical-scientific associations and the pharmaceutical industry, which tends to present male aging as a medical problem and promotes hormone replacement therapy (HRT) with testosterone as a way of treating it. This therapy is also presented as a means to recover happiness, productivity, „quality of life‟ and wellbeing.
Methods: The experimental study included 48 male Wistar albino rats (body weight 200 to 250 g). The rats were randomized into four groups of 12 rats each. The control group was given commercial drinking water, and the experimental groups were given 20 g/L M. piperita tea, 20 g/L M. spicata tea, or 40 g/L M. spicata tea. Results: The follicle-stimulating hormone and luteinizing hormone levels had increased and total testosterone levels had decreased in the experimental groups compared with the control group; the differences were statistically significant. Also, the Johnsen testicular biopsy scores were significantly different statistically between the experimental groups and the control group. Although the mean seminiferous tubular diameter of the experimental groups was relatively greater than in the control group, the difference was not statistically significant. The only effects of M. piperita on testicular tissue was segmental maturation arrest in the seminiferous tubules; however, the effects of M. spicata extended from maturation arrest to diffuse germ cell aplasia in relation to the dose.
Durante a puberdade, eleva-se a secreção de três hormônios: os esteróides sexuais, o hormônio de crescimento (GH , growth hormone) e o IGF-1. A seqüência de intervenção de cada um deles na acele- ração estatural não está bem esclarecida. H á um aumento na amplitude dos picos de GH e da quanti- dade total de GH secretado, sem modificação na fre- qüência desses picos (7). O mecanismo pelo qual os esteróides sexuais aumentam a secreção de GH é impreciso. Em adolescentes com atraso puberal, a diminuição na secreção de GH parece resultar da diminuição do seu estimulador hipotalâmico, o GH RH (GH releasing hormone) (8). Normalmente, a secreção de GH RH aumenta durante a puberdade, enquanto a de somatostatina se mantém estável. O s níveis plasmáticos de GH BP (growth hormone binding
Resistance to thyroid hormone (RTH) is a syndrome characterized by ele- vated serum thyroid hormone (TH) levels and elevated or inappropriate- ly normal thyrotropin levels. In general, patients exhibit TH resistance in the pituitary and peripheral tissues. The phenotype of RTH is variable; the affected individuals are clinically euthyroid or even hypothyroid depend- ing on the severity of the mutation, the variable hyposensitivity to TH among individuals as well as in different tissues. In almost all cases the genetic basis of RTH lies in mutation of the carboxyl-terminus of the β-thy- roid hormone receptor. RTH is a dominant disorder, except in one family; most individuals are heterozygous for the mutant allele. New standard techniques and genetically engineered mouse model systems have increased our understanding on TH receptor action, in particular, how mutant thyroid receptors from RTH patients can block wild-type thyroid receptor function (dominant negative activity), and how the mutant receptors can differently affect various tissues and individuals. (Arq Bras Endocrinol Metab 2004;48/1:83-92)
The aim of this study was to evaluate the influence of terminal liver disease and OLT in the pituitary function and hormone metabolism by measurement of serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2) and prolactin (PRL) before and after liver transplantation.
Crianças com doenças crônicas freqüentemente apresentam crescimento inadequado e baixa estatura. A falência do crescimento é multifatorial. Nas doenças inflamatórias, como na artrite juvenil idiopática e nas doenças infla- matórias intestinais, o crescimento é comprometido também pelo processo inflamatório. Muitas vezes, o tratamento da doença de base compromete o crescimento, especialmente quando é necessário glicocorticóides. Em algu- mas situações é possível comprovar a deficiência associada de hormônio de crescimento (GH, do inglês growth hormone). Em outras, os exames suge- rem certo grau de insensibilidade ao GH. O tratamento destes pacientes com GH tem se mostrado útil e seguro com melhora do crescimento e da quali- dade de vida. Nesta revisão, são apresentados resultados do tratamento com GH em pacientes com baixa estatura decorrente de doenças crônicas, algu- mas indicações já bem definidas e outras ainda em investigação. (Arq Bras Endocrinol Metab 2008; 52/5:774-782)
TW generally have a psychological need to increase estrogen replacement doses to acquire a female phenotype as soon as possible. A higher estrogen dose is associated with an increased risk of venous thromboembolic disease, pul- monary embolism, myocardial infarction, stroke, hormone- related tumors and adverse liver effects (17). In addition to these common side effects of high-dose estrogen therapy, increases in PRL levels and even prolactinoma development have been described in TW (18-24).
We evaluated 907 men who were referred to our institution for prostate cancer screening in March 2012. Men with more than 50 years were eligible to participate. All patients were initially attended by a nurse responsible for assess their vital signs (temperature, blood pressure, heart beat rate, and glucose level). Patient’s height and wei- ght were also measured. All patients also filled out a questionnaire with their demographic data. Be- fore medical visit, blood tests were collected and it could include the reproductive hormone profile if patients were in agreement. Eight hundred and se- venty five men signed the consent term and were enrolled in this study. Institutional Review Board and Human Subjects Committee approved it.
A systematic review of the literature assessing several markers of OVR in the assisted reproductive technology setting was published in 2006. 2 Levels of estradiol, the ﬁrst marker assessed, were not shown to be effective predictors of OVR-related outcomes, even when combined with other markers. 3 Follicle-stimulating hormone measurements are affected only when OVR is critically jeopardized. 4,5 In a 2002 study of potential predictors of poor response to ovarian stimulation for in vitro fertilization (IVF) cycles, Bancsi et al 3 showed that AFC alone provided the best prognostic value as compared with FSH, inhibin B, and estradiol.