scholarly journals Pituitary Hyperplasia, Hormonal Changes and Prolactinoma Development in Males Exposed to Estrogens—An Insight From Translational Studies

2020 ◽  
Vol 21 (6) ◽  
pp. 2024 ◽  
Author(s):  
Branka Šošić-Jurjević ◽  
Vladimir Ajdžanović ◽  
Dragana Miljić ◽  
Svetlana Trifunović ◽  
Branko Filipović ◽  
...  
Keyword(s):  
Human Subjects ◽  
Secretory Activity ◽  
Estrogen Signaling ◽  
Hormonal Changes ◽  
Estrogen Action ◽  
Pituitary Development ◽  
Pituitary Hyperplasia ◽  
Male Animal ◽  
Male Patients ◽  
And Function

Estrogen signaling plays an important role in pituitary development and function. In sensitive rat or mice strains of both sexes, estrogen treatments promote lactotropic cell proliferation and induce the formation of pituitary adenomas (dominantly prolactin or growth-hormone-secreting ones). In male patients receiving estrogen, treatment does not necessarily result in pituitary hyperplasia, hyperprolactinemia or adenoma development. In this review, we comprehensively analyze the mechanisms of estrogen action upon their application in male animal models comparing it with available data in human subjects. Sex-specific molecular targets of estrogen action in lactotropic (PRL) cells are highlighted in the context of their proliferative and secretory activity. In addition, putative effects of estradiol on the cellular/tumor microenvironment and the contribution of postnatal pituitary progenitor/stem cells and transdifferentiation processes to prolactinoma development have been analyzed. Finally, estrogen-induced morphological and hormone-secreting changes in pituitary thyrotropic (TSH) and adrenocorticotropic (ACTH) cells are discussed, as well as the putative role of the thyroid and/or glucocorticoid hormones in prolactinoma development, based on the current scarce literature.

CHANGES IN THE CONCENTRATION OF PITUITARY AND STEROID HORMONES IN THE FOLLICULAR FLUID OF HUMAN GRAAFIAN FOLLICLES THROUGHOUT THE MENSTRUAL CYCLE

1975 ◽  
Vol 64 (3) ◽  
pp. 555-571 ◽  
Author(s):  
K. P. McNATTY ◽  
W. M. HUNTER ◽  
A. S. McNEILLY ◽  
R. S. SAWERS
Keyword(s):  
Menstrual Cycle ◽  
Steroid Hormones ◽  
Follicular Fluid ◽  
Follicle Stimulating Hormone ◽  
Secretory Activity ◽  
Follicular Phase ◽  
Hormonal Changes ◽  
Peripheral Plasma ◽  
Before And After ◽  
Late Follicular Phase

SUMMARY The concentrations of FSH, LH, prolactin, oestradiol and progesterone were measured in peripheral plasma and follicular fluid of women throughout the menstrual cycle. With the exception of prolactin, concentrations of pituitary and steroid hormones in follicular fluid correlated with those in peripheral plasma. Follicle-stimulating hormone was present in a greater number of small follicles ( < 8 mm) during or just after the peaks of FSH in peripheral plasma. During the mid-follicular phase the concentration of both FSH and oestradiol in fluid from large follicles ( ≥ 8 mm) was high. During the late follicular phase the large follicles ( ≥ 8 mm) contained high amounts of progesterone in addition to oestradiol, low physiological levels of prolactin, and concentrations of LH and FSH about 30 and 60% respectively of those found in plasma. By contrast no large 'active' follicles ( ≥ 8 mm) were found during the luteal phase although many contained both LH and FSH. Luteinizing hormone was present in a proportion of small follicles ( < 8 mm) during the late follicular and early luteal but not at other stages of the menstrual cycle. It is suggested that a precise sequence of hormonal changes occur within the microenvironment of the developing Graafian follicle; the order in which they occur may be of considerable importance for the growth of that follicle and secretory activity of the granulosa cells both before and after ovulation.

Right ventricle dimensions and function in response to acute hypoxia in healthy human subjects

2016 ◽  
Vol 219 (2) ◽  
pp. 478-485 ◽  
Author(s):  
N. C. Netzer ◽  
K. P. Strohl ◽  
J. Högel ◽  
H. Gatterer ◽  
R. Schilz
Keyword(s):  
Right Ventricle ◽  
Human Subjects ◽  
Acute Hypoxia ◽  
Healthy Human ◽  
Healthy Human Subjects ◽  
And Function

Chronic exercise and left ventricular structure and function in healthy human subjects

1985 ◽  
Vol 58 (2) ◽  
pp. 409-415 ◽  
Author(s):  
L. A. Wolfe ◽  
R. P. Martin ◽  
D. D. Watson ◽  
R. D. Lasley ◽  
D. E. Bruns
Keyword(s):  
Human Subjects ◽  
Exercise Program ◽  
Left Ventricular ◽  
Control Group ◽  
Healthy Human ◽  
Mean Values ◽  
End Diastolic Volume ◽  
Supervised Exercise ◽  
Fitness Training ◽  
And Function

Twelve healthy well-trained participants in a supervised exercise program (mean age, 41.3 yr) were compared with 12 sedentary control subjects (mean age, 38.9 yr) with physical characteristics similar to the exercised group (EG) before training. Resting echocardiograms revealed significantly lower heart rates (HR) in the EG compared with control group (CG) but no evidence for cardiac structural differences between groups. Radionuclide angiograms performed at rest and during two levels of supine cycling (HR targets: 120 and 140 beats X min-1) resulted in increases in background-corrected end-diastolic counts [EDC(bc)] and confirmed use of the Frank-Starling mechanism in the majority of subjects. Mean values (+/- SD) for ejection fraction (EF) and normalized peak systolic ejection rate (PSER) (P greater than 0.05 between groups) were the following. (Formula: see text) The results suggested that fitness training does not induce significant cardiac enlargement as apparent from measurements at rest or important changes in contractile state during exercise. Increases in exercise stroke volume with such training may be the result of an increased end-diastolic volume.

scholarly journals Silence, Solitude, and Serotonin: Neural Mechanisms Linking Hearing Loss and Social Isolation

2020 ◽  
Vol 10 (6) ◽  
pp. 367
Author(s):  
Sarah M. Keesom ◽  
Laura M. Hurley
Keyword(s):  
Hearing Loss ◽  
Social Isolation ◽  
Human Subjects ◽  
Brain Regions ◽  
Neural Systems ◽  
Depression And Anxiety ◽  
Auditory Cognition ◽  
Regulatory Systems ◽  
Two Factors ◽  
And Function

For social animals that communicate acoustically, hearing loss and social isolation are factors that independently influence social behavior. In human subjects, hearing loss may also contribute to objective and subjective measures of social isolation. Although the behavioral relationship between hearing loss and social isolation is evident, there is little understanding of their interdependence at the level of neural systems. Separate lines of research have shown that social isolation and hearing loss independently target the serotonergic system in the rodent brain. These two factors affect both presynaptic and postsynaptic measures of serotonergic anatomy and function, highlighting the sensitivity of serotonergic pathways to both types of insult. The effects of deficits in both acoustic and social inputs are seen not only within the auditory system, but also in other brain regions, suggesting relatively extensive effects of these deficits on serotonergic regulatory systems. Serotonin plays a much-studied role in depression and anxiety, and may also influence several aspects of auditory cognition, including auditory attention and understanding speech in challenging listening conditions. These commonalities suggest that serotonergic pathways are worthy of further exploration as potential intervening mechanisms between the related conditions of hearing loss and social isolation, and the affective and cognitive dysfunctions that follow.

scholarly journals Myostatin regulates pituitary development and hepatic IGF1

2019 ◽  
Vol 316 (6) ◽  
pp. E1036-E1049 ◽  
Author(s):  
Wioletta Czaja ◽  
Yukiko K. Nakamura ◽  
Naisi Li ◽  
Jennifer A. Eldridge ◽  
David M. DeAvila ◽  
...  
Keyword(s):  
Striated Muscle ◽  
Muscle Growth ◽  
Unintended Consequences ◽  
Pituitary Development ◽  
Igf Binding ◽  
Acid Labile Subunit ◽  
Muscle Wasting Disease ◽  
And Function ◽  
Igf Binding Protein ◽  
Igf1 Expression

Circulating myostatin-attenuating agents are being developed to treat muscle-wasting disease despite their potential to produce serious off-target effects, as myostatin/activin receptors are widely distributed among many nonmuscle tissues. Our studies suggest that the myokine not only inhibits striated muscle growth but also regulates pituitary development and growth hormone (GH) action in the liver. Using a novel myostatin-null label-retaining model (Jekyll mice), we determined that the heterogeneous pool of pituitary stem, transit-amplifying, and progenitor cells in Jekyll mice depletes more rapidly after birth than the pool in wild-type mice. This correlated with increased levels of GH, prolactin, and the cells that secrete these hormones, somatotropes and lactotropes, respectively, in Jekyll pituitaries. Recombinant myostatin also stimulated GH release and gene expression in pituitary cell cultures although inhibiting prolactin release. In primary hepatocytes, recombinant myostatin blocked GH-stimulated expression of two key mediators of growth, insulin-like growth factor (IGF)1 and the acid labile subunit and increased expression of an inhibitor, IGF-binding protein-1. The significance of these findings was demonstrated by smaller muscle fiber size in a model lacking myostatin and liver IGF1 expression (LID-o-Mighty mice) compared with that in myostatin-null (Mighty) mice. These data together suggest that myostatin may regulate pituitary development and function and that its inhibitory actions in muscle may be partly mediated by attenuating GH action in the liver. They also suggest that circulating pharmacological inhibitors of myostatin could produce unintended consequences in these and possibly other tissues.

scholarly journals Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer

2016 ◽  
Vol 2 (6) ◽  
pp. e1501924 ◽  
Author(s):  
Hari Singhal ◽  
Marianne E. Greene ◽  
Gerard Tarulli ◽  
Allison L. Zarnke ◽  
Ryan J. Bourgo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Target Genes ◽  
Tumor Regression ◽  
Progesterone Receptors ◽  
Estrogen Signaling ◽  
Breast Cancers ◽  
Estrogen Action ◽  
Cellular Processes ◽  
Estrogen Receptor Positive ◽  
Estrogen Antagonist

The functional role of progesterone receptor (PR) and its impact on estrogen signaling in breast cancer remain controversial. In primary ER+ (estrogen receptor–positive)/PR+ human tumors, we report that PR reprograms estrogen signaling as a genomic agonist and a phenotypic antagonist. In isolation, estrogen and progestin act as genomic agonists by regulating the expression of common target genes in similar directions, but at different levels. Similarly, in isolation, progestin is also a weak phenotypic agonist of estrogen action. However, in the presence of both hormones, progestin behaves as a phenotypic estrogen antagonist. PR remodels nucleosomes to noncompetitively redirect ER genomic binding to distal enhancers enriched for BRCA1 binding motifs and sites that link PR and ER/PR complexes. When both hormones are present, progestin modulates estrogen action, such that responsive transcriptomes, cellular processes, and ER/PR recruitment to genomic sites correlate with those observed with PR alone, but not ER alone. Despite this overall correlation, the transcriptome patterns modulated by dual treatment are sufficiently different from individual treatments, such that antagonism of oncogenic processes is both predicted and observed. Combination therapies using the selective PR modulator/antagonist (SPRM) CDB4124 in combination with tamoxifen elicited 70% cytotoxic tumor regression of T47D tumor xenografts, whereas individual therapies inhibited tumor growth without net regression. Our findings demonstrate that PR redirects ER chromatin binding to antagonize estrogen signaling and that SPRMs can potentiate responses to antiestrogens, suggesting that cotargeting of ER and PR in ER+/PR+ breast cancers should be explored.

scholarly journals Hormonal alterations in PCOS and its influence on bone metabolism

2017 ◽  
Vol 232 (2) ◽  
pp. R99-R113 ◽  
Author(s):  
Abhaya Krishnan ◽  
Sridhar Muthusami
Keyword(s):  
Bone Metabolism ◽  
Polycystic Ovary ◽  
Human Subjects ◽  
The United States ◽  
Reproductive Age ◽  
World Health ◽  
Hormonal Changes ◽  
Mineral Density ◽  
Hormonal Imbalance ◽  
Health Organization

According to the World Health Organization (WHO) polycystic ovary syndrome (PCOS) occurs in 4–8% of women worldwide. The prevalence of PCOS in Indian adolescents is 12.2% according to the Indian Council of Medical Research (ICMR). The National Institute of Health has documented that it affects approximately 5 million women of reproductive age in the United States. Hormonal imbalance is the characteristic of many women with polycystic ovarian syndrome (PCOS). The influence of various endocrine changes in PCOS women and their relevance to bone remains to be documented. Hormones, which include gonadotrophin-releasing hormone (GnRH), insulin, the leutinizing/follicle-stimulating hormone (LH/FSH) ratio, androgens, estrogens, growth hormones (GH), cortisol, parathyroid hormone (PTH) and calcitonin are disturbed in PCOS women. These hormones influence bone metabolism in human subjects directly as well as indirectly. The imbalance in these hormones results in increased prevalence of osteoporosis in PCOS women. Limited evidence suggests that the drugs taken during the treatment of PCOS increase the risk of bone fracture in PCOS patients through endocrine disruption. This review is aimed at the identification of the relationship between bone mineral density and hormonal changes in PCOS subjects and identifies potential areas to study bone-related disorders in PCOS women.

scholarly journals Ozone: A Review of Recent Experimental, Clinical and Epidemiological Evidence, with Notes on Causation—Part 1

1995 ◽  
Vol 2 (1) ◽  
pp. 25-31 ◽  
Author(s):  
David V Bates
Keyword(s):  
Clinical Studies ◽  
Animal Studies ◽  
Human Subjects ◽  
Ozone Exposure ◽  
Long Term Effects ◽  
Mechanisms Of Adaptation ◽  
Living Tissues ◽  
And Function ◽  
Theoretical Issues

Part 1 of this review is concerned with theoretical issues of ozone dosimetry, animal and cellular studies that illustrate the mechanism of action of ozone on living tissues, and with clinical studies. Animal studies have indicated that there are long term effects from low level long term ozone exposure. Clinical studies involve controlled ozone exposures on human subjects, both normals and asthmatics. Exercise concomitant with the ozone exposure increases the effect of the gas. It is concluded that the induction of an inflammatory response in the airway, both in the nose and in the lung, is the striking and earliest feature of ozone exposure. Current unexplained observations include: the dissociation between the inflammatory and function test response; the mechanisms of ‘adaptation’ and of airway hyperresponsiveness; and the phenomena that underlie the effect of ozone on maximal athletic performance.

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