PROFILE OF SEX STEROIDS AT EARLY STAGES OF LIVER METASTASIS FROM SARCOMA 45 IN MALE RATS

e23010 Background: Numerous clinical studies have shown an association between changing thyroid gland (TG) function and the development of tumors. The purpose of the study was to analyze the dynamics of thyroid hormones in the pituitary gland, TG and blood serum (BS) during liver metastasis in order to create thyroid profile of metastasis and to detect thyroid markers of metastasis in BS. Methods: The experiment included 44 white male rats weighing 180-250 g. Sarcoma 45 was transplanted intrasplenically. Levels of thyroid stimulating hormone (TSH) were studied in the pituitary gland, TG, BS; the amount of free (fT4) and total (T4) thyroxine and free (fT3) and total (T3) triiodothyronine in TG and BS were determined by radioimmunoassay (Immunotech, Czech Republic; Arian analyzer, Russia). Results: Exertion of the pituitary gland and overproduction of TSH were observed since the early days of the tumor development, later accompanied by TG hypofunction. Quantitative changes of thyroid hormones in organs did not coincide with their dynamics in BS. The first diagnostic signs of experimental liver metastasis, in the absence of formed metastases in the body, were hyperthyrotropinemia and a tendency to fT3 decrease in BS. Already formed liver metastases were characterized by a marked low T3 syndrome which transformed into a more severe lowT3/lowT4 syndrome during the secondary metastasis. Conclusions: The development of liver metastases is accompanied by the exertion and imbalance of the thyroid system function. Analysis of dynamics of the thyroid axis hormones in BS allows predicting the appearance of liver metastasis and identification of “the point of no return” in the development of the pathology that leads to secondary metastasis and irreversible progression of the disease.

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Effects of Castration, Sex Steroids, LHRH and Glucocorticoids on LHRH Binding in the Anterior Pituitary of Male Rats

The Journal of Urology ◽

10.1016/s0022-5347(17)52842-6 ◽

1982 ◽

Vol 128 (1) ◽

pp. 224-224

Author(s):

O. Naess ◽

L. Cusan ◽

I. Brekke ◽

K. Purvis ◽

P. Torjesen ◽

...

Keyword(s):

Sex Steroids ◽

Anterior Pituitary ◽

Male Rats

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Effects of Sex Steroids on Secretory Granule Formation in Gonadotropes of Castrated Male Rats with Respect to Granin Expression*

Endocrinology ◽

10.1210/endo.139.6.6059 ◽

1998 ◽

Vol 139 (6) ◽

pp. 2765-2773 ◽

Cited By ~ 10

Author(s):

Tsuyoshi Watanabe ◽

Tomohiro Banno ◽

Thomas Jeziorowski ◽

Yoshiyuki Ohsawa ◽

Satoshi Waguri ◽

...

Keyword(s):

Sex Steroids ◽

Plasma Levels ◽

Chromogranin A ◽

Secretory Granules ◽

Male Rats ◽

Female Rat ◽

Granule Formation ◽

Male And Female ◽

Immunocytochemical Studies ◽

Circulating Levels

Abstract Pituitary gonadotropes show sex-related differences in their ultrastructure. Typical gonadotropes of male rats exhibit both large granules, which contain chromogranin A (CgA), and small granules, which contain secretogranin II (SgII). In contrast, typical female rat gonadotropes show only a very few large granules among the numerous small granules. To clarify the nature of the biogenesis of these secretory granules and the effects of sex steroids, the ultrastructural and immunocytochemical changes in gonadotropes were examined in castrated male rats supplied with a testosterone or estradiol implant. In castrated rats, pituitary expression and plasma levels of LH increased drastically, but the pituitary content of CgA decreased. The majority of gonadotropes then showed features of “castration cells” containing many small secretory granules. A testosterone implant to castrated rats remarkably suppressed the expression and circulating levels of LH and increased the CgA content in the pituitary to near-normal levels. In this situation, immunocytochemical studies demonstrated that gonadotropes again exhibited large and small secretory granules with the respective localization of CgA and SgII. On the contrary, in castrated rats supplied with an estradiol implant, the expression and content of CgA in the pituitary were remarkably suppressed, and large secretory granules disappeared from gonadotropes. These results suggest that the expression of CgA in gonadotropes is regulated differently by male and female sex steroids. These different effects of androgen and estrogen on the expression level of CgA are closely associated with the sex-related differences in the ultrastructure of secretory granules within gonadotropes.

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Opposite Effects of Androgens and Estrogens on Adipogenesis in Rat Preadipocytes: Evidence for Sex and Site-Related Specificities and Possible Involvement of Insulin-Like Growth Factor 1 Receptor and Peroxisome Proliferator-Activated Receptorγ 21

Endocrinology ◽

10.1210/endo.141.2.7293 ◽

2000 ◽

Vol 141 (2) ◽

pp. 649-656 ◽

Cited By ~ 103

Author(s):

M. N. Dieudonne ◽

R. Pecquery ◽

M. C. Leneveu ◽

Y. Giudicelli

Keyword(s):

Growth Factor ◽

Dehydrogenase Activity ◽

Sex Steroids ◽

Female Rats ◽

Male Rats ◽

Ovariectomized Rats ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

17Β Estradiol ◽

Glycerol 3 Phosphate Dehydrogenase

Abstract To investigate the role of sex steroid hormones in adipose tissue development and distribution, we have studied the effect of various sex steroids (testosterone, dihydrotestosterone (DHT), and 17β-estradiol) in vitro, on the proliferation and differentiation processes in rat preadipocytes from deep (epididymal and parametrial) and superficial (femoral sc) fat deposits. All added steroids failed to affect the growth rate of preadipocytes from male rats when determined from day 1 to day 4 after plating, whether FCS was present or not in the culture medium. In contrast, in preadipocytes from female rats, we observed a positive effect (×2) of 17β-estradiol (0.01μ m) on the proliferative capacities of sc but not parametrial preadipocytes. When preadipocytes were exposed to testosterone or DHT (0.1 μm) during the differentiation process, the glycerol 3-phosphate dehydrogenase activity was significantly decreased in epididymal preadipocytes only. When preadipocytes from male rats were exposed to 17β-estradiol (0.01μ m), the differentiation capacities of preadipocytes were not modified. However, in parametrial preadipocytes from ovariectomized female rats, 17β-estradiol significantly increased (×1.34) the glycerol 3-phosphate dehydrogenase activity. In differentiated preadipocytes that had been exposed to sex steroids, expression of peroxisome proliferator-activated receptor γ2 was up-regulated by 17β-estradiol but not by androgens. As described in other cell types, sex steroids modulate insulin growth factor 1 receptor (IGF1R) expression in preadipocytes. Indeed, IGF1R levels were either enhanced by 17 β-estradiol (0.01 μm) in sc preadipocytes from female ovariectomized rats or decreased by DHT (0.01 μm) in epididymal preadipocytes. These effects were reversed by simultaneous exposure to androgen or estrogen receptor antagonists. In conclusion, this study demonstrates that, in rat preadipocytes kept in primary culture and chronically exposed to sex hormones, androgens elicit an antiadipogenic effect, whereas estrogens behave as proadipogenic hormones. Moreover, our results suggest that these opposite effects could be related to changes in IGF1R (androgens and estrogens) and peroxisome proliferator-activated receptor γ2 expression (estrogens).

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Effects of castration, sex steroids, LHRH and glucocorticoids on LHRH binding in the anterior pituitary of male rats

International Journal of Andrology ◽

10.1111/j.1365-2605.1981.tb00752.x ◽

1981 ◽

Vol 4 (1-6) ◽

pp. 685-690 ◽

Cited By ~ 6

Author(s):

Oddvar Naess ◽

Lionel Cusan ◽

Inger Brekke ◽

Kenneth Purvis ◽

Peter Torjesen ◽

...

Keyword(s):

Sex Steroids ◽

Anterior Pituitary ◽

Male Rats

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Early Long-Term Memory Impairment and Changes in the Expression of Synaptic Plasticity-Associated Genes, in the McGill-R-Thy1-APP Rat Model of Alzheimer's-Like Brain Amyloidosis

Frontiers in Aging Neuroscience ◽

10.3389/fnagi.2020.585873 ◽

2021 ◽

Vol 12 ◽

Author(s):

Martín Habif ◽

Sonia Do Carmo ◽

María Verónica Báez ◽

Natalia Claudia Colettis ◽

Magalí Cecilia Cercato ◽

...

Keyword(s):

Synaptic Plasticity ◽

Learning And Memory ◽

Memory Deficits ◽

Male Rats ◽

Long Term Memory ◽

Aβ Oligomers ◽

Term Memory ◽

Early Stages ◽

Human Pathology

Accruing evidence supports the hypothesis that memory deficits in early Alzheimer Disease (AD) might be due to synaptic failure caused by accumulation of intracellular amyloid beta (Aβ) oligomers, then secreted to the extracellular media. Transgenic mouse AD models provide valuable information on AD pathology. However, the failure to translate these findings to humans calls for models that better recapitulate the human pathology. McGill-R-Thy1-APP transgenic (Tg) rat expresses the human amyloid precursor protein (APP751) with the Swedish and Indiana mutations (of familial AD), leading to an AD-like slow-progressing brain amyloid pathology. Therefore, it offers a unique opportunity to investigate learning and memory abilities at early stages of AD, when Aβ accumulation is restricted to the intracellular compartment, prior to plaque deposition. Our goal was to further investigate early deficits in memory, particularly long-term memory in McGill-R-Thy1-APP heterozygous (Tg+/–) rats. Short-term- and long-term habituation to an open field were preserved in 3-, 4-, and 6-month-old (Tg+/–). However, long-term memory of inhibitory avoidance to a foot-shock, novel object-recognition and social approaching behavior were seriously impaired in 4-month-old (Tg+/–) male rats, suggesting that they are unable to either consolidate and/or evoke such associative and discriminative memories with aversive, emotional and spatial components. The long-term memory deficits were accompanied by increased transcript levels of genes relevant to synaptic plasticity, learning and memory processing in the hippocampus, such as Grin2b, Dlg4, Camk2b, and Syn1. Our findings indicate that in addition to the previously well-documented deficits in learning and memory, McGill-R-Thy1-APP rats display particular long-term-memory deficits and deep social behavior alterations at pre-plaque early stages of the pathology. This highlights the importance of Aβ oligomers and emphasizes the validity of the model to study AD-like early processes, with potentially predictive value.

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Darapladib inhibits atherosclerosis development in type 2 diabetes mellitus Sprague-Dawley rat model

Endocrine Regulations ◽

10.2478/enr-2018-0008 ◽

2018 ◽

Vol 52 (2) ◽

pp. 69-75 ◽

Cited By ~ 2

Author(s):

Titin Andri Wihastuti ◽

Teuku Heriansyah ◽

Hanifa Hanifa ◽

Sri Andarini ◽

Zuhrotus Sholichah ◽

...

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Rat Model ◽

Foam Cells ◽

Male Rats ◽

Sprague Dawley ◽

Early Stages ◽

Sprague Dawley Rat

AbstractObjective. Increase in the low-density lipoprotein (LDL) level in diabetes mellitus and atherosclerosis is related to lipoprotein associated phospholipase A2 (Lp-PLA2). Lp-PLA2 is an enzyme that produces lysophosphatidylcholine (LysoPC) and oxidized nonesterified fatty acids (oxNEFA). LysoPC regulates inflammation mediators, including intra-cellular adhesion molecule-1 (ICAM-1). Darapladib is known as a Lp-PLA2 specific inhibitor. The aim of this study was to reveal the effect of darapladib on the foam cell number, inducible nitric oxide synthase (iNOS), and ICAM-1 expression in aorta at early stages of the atherosclerosis in type 2 diabetes mellitus Sprague-Dawley rat model.Methods. Thirty Sprague-Dawley male rats were divided into 3 main groups: control, rats with type 2 diabetes mellitus (T2DM), and T2DM rats treated with darapladib (T2DM-DP). Each group was divided into 2 subgroups according the time of treatment: 8-week and 16-week treatment group. Fasting blood glucose, insulin resistance, and lipid profile were measured and analyzed to ensure T2DM model. The foam cells number were detected using hematoxylin-eosin (HE) staining and the expression of iNOS and ICAM-1 was analyzed using double immunofluorescence staining.Results. Induction of T2DM in male Sprague-Dawley rats after high fat diet and streptozotocin injection was confirmed by elevated levels of total cholesterol and LDL and increased fasting glucose and insulin levels compared to controls after both times of treatment. Moreover, T2DM in rats induced a significant increase (p<0.05) in the foam cells number and iNOS and ICAM-1 expression in aorta compared to controls after both treatment times. Darapladib treatment significantly reduced (p<0.05) foam cells number as well as iNOS expression in aorta in rats with T2DM after both treatment times. A significant decrease (p<0.05) in ICAM-1 expression in aorta was observed after darapladib treatment in rats with T2DM only after 8 weeks of treatment.Conclusion. Our data indicate that darapladib can decrease the foam cells number, iNOS, and ICAM-1 expression in aorta at the early stages of atherosclerosis in T2DM rat model.

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