Testosterone and estradiol differentially regulate TSH-induced thyrocyte proliferation in immature and adult rats

Banu, Sakhila K.; Govindarajulu, P.; Aruldhas, M. M.

doi:10.1016/s0039-128x(02)00008-9

Cited by 34 publications

(27 citation statements)

References 21 publications

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“…Eight-day-old rats show lower amounts of circulating sex hormones than 15-day ones similar to adult as already reported (Banu et al 2002, Zapatero-Caballero et al 2004. Also in these experimental models, HMG-CoAR and INSIG protein levels were studied.…”

Section: Sex Differences During Rat Developmentsupporting

confidence: 51%

“…In fact, 15-day-old rats are characterized by a physiological burst of sex hormones that reach the same plasma concentration as adults (Banu et al 2002, Zapatero-Caballero et al 2004 and show an expression pattern of studied proteins comparable with that of adult rats. When testosterone peak is present (15-day old), no change in HMGCoAR levels are observable in males since, in fact, 8-day-to 3-month-old HMG-CoAR levels do not change in males.…”

Section: Discussionmentioning

confidence: 98%

“…Then, we evaluated the protein levels in males and females, 8-and 15-day old, representing two developmental stages where serum estradiol and testosterone levels in female and in male respectively are physiologically modified (Banu et al 2002, Zapatero-Caballero et al 2004. Finally, the direct estrogen effects were evaluated treating adult male rats with pharmacological doses of 17-b-estradiol, contributing to better understanding estrogen involvement in these mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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Sex differences in hepatic regulation of cholesterol homeostasis

Marinis¹,

Martini²,

Trentalance³

et al. 2008

Journal of Endocrinology

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Physiological sex differences may influence metabolic status and then alter the onset of some diseases. According to recent studies, it is now well established that females are more protected from hypercholesterolemia-related diseases, such as cardiovascular diseases until menopause. Female protection from hypercholesterolemia is mediated by the hypolipidemic properties of estrogens, even if mechanisms underlying this protection remain still debated. Even though the regulatory mechanisms of cholesterol homeostasis maintenance are well known, few data are available on the supposed differences between male and female in these processes. So, the aim of this work was to define, through an in vivo study, the putative sex-dependent regulation of the processes underlying cholesterol homeostasis maintenance. We examined 3-hydroxy 3-methylglutaryl coenzyme A reductase and its regulatory protein network as well as the amount of low-density lipoprotein receptor and cholesterol. The study was conducted in the liver and plasma of male and female rats, on adults and during postnatal development, and on 17-b-estradiol-treated male rats. Our data support that physiological differences in proteins involved in cholesterol balance are present between the sexes and, in particular, 3-hydroxy 3-methylglutaryl coenzyme A reductase shows lower activity and expression in female and 17-b-estradioltreated male rats than in adult untreated male. Our data suggest that sex differences in enzyme expression depend on variation in regulatory proteins and seem to be related to estrogen presence. This work adds new evidence in the complicated picture of sex-dependent cellular physiology and establishes a new role for reductase regulatory proteins as a link between estrogen protective effects and cholesterol homeostasis.

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Section: Sex Differences During Rat Developmentsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Sex differences in hepatic regulation of cholesterol homeostasis

Marinis¹,

Martini²,

Trentalance³

et al. 2008

Journal of Endocrinology

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“…In addition to satellite cells, AR is expressed in mature myofibers (Saartok et al 1984, Sar et al 1990) in several types of motoneurons (Lumbroso et al 1996, Piccioni et al 2001, and in intramuscular fibroblasts (Monks et al 2004), and thus could influence growth and function through activation in these cells. Finally, androgens regulate systemic levels of IGF1, GH, and thyroid hormone, and may oppose the actions of glucocorticoids, any of which could contribute to the effects of androgen on muscle (Link et al 1986, Hickson et al 1990, Banu et al 2002, Ferrando et al 2002.…”

Section: Introductionmentioning

confidence: 99%

Androgen-mediated improvement of body composition and muscle function involves a novel early transcriptional program including IGF1, mechano growth factor, and induction of β-catenin

Gentile¹,

Nantermet²,

Vogel³

et al. 2009

Journal of Molecular Endocrinology

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Androgens promote anabolism in the musculoskeletal system while generally repressing adiposity, leading to lean body composition. Circulating androgens decline with age, contributing to frailty, osteoporosis, and obesity; however, the mechanisms by which androgens modulate body composition are largely unknown. Here, we demonstrate that aged castrated rats develop increased fat mass, reduced muscle mass and strength, and lower bone mass. Treatment with testosterone or 5a-dihydrotestosterone (DHT) reverses the effects on muscle and adipose tissues while only aromatizable testosterone increased bone mass. During the first week, DHT transiently increased soleus muscle nuclear density and induced expression of IGF1 and its splice variant mechano growth factor (MGF) without early regulation of the myogenic factors MyoD, myogenin, monocyte nuclear factor, or myostatin. A genome-wide microarray screen was also performed to identify potential pro-myogenic genes that respond to androgen receptor activation in vivo within 24 h. Of 24 000 genes examined, 70 candidate genes were identified whose functions suggest initiation of remodeling and regeneration, including the type II muscle genes for myosin heavy chain type II and parvalbumin and the chemokine monocyte chemoattractant protein-1. Interestingly, Axin and Axin2, negative regulators of b-catenin, were repressed, indicating modulation of the b-catenin pathway. DHT increased total levels of b-catenin protein, which accumulated in nuclei in vivo. Likewise, treatment of C2C12 myoblasts with both IGF1Ea and MGF C-terminal peptide increased nuclear b-catenin in vitro. Thus, we propose that androgenic anabolism involves early downregulation of Axin and induction of IGF1, leading to nuclear accumulation of b-catenin, a pro-myogenic, anti-adipogenic stem cell regulatory factor.

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“…demonstraram que os esteróides sexuais, masculino e feminino, exercem papel fundamental na regulação da resposta proliferativa ao TSH, pois em animais gonadectomizados essa resposta estava suprimida (31). Em outro estudo, esses autores demonstraram que a testosterona é um potente fator mitogênico nos tireócitos em cultura, atuando em conjunto com o TSH ou não (32). Borges e cols.…”

Section: Esteróides Anabolizantes X Função Tireóideaunclassified

Abuso de esteróides anabolizantes e seu impacto sobre a função tireóidea

Fortunato

Rosenthal

Carvalho

et al. 2007

Arq Bras Endocrinol Metab

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A utilização de esteróides anabolizantes por indivíduos que desejam aumentar sua performance física, ou simplesmente para fins estéticos, tem atingido índices alarmantes nas últimas três décadas. Além dos efeitos desejados, uma infinidade de efeitos colaterais já foi bem descrita na literatura, como vários tipos de câncer, ginecomastia, peliosis hepatis, insuficiência renal, virilização, dentre outros. Sobre a função tireóidea, o efeito mais pronunciado em seres humanos é a diminuição da TBG, com conseqüente diminuição sérica de T3 e T4 totais, dependendo, porém, da susceptibilidade da molécula à aromatização e conseqüente transformação em estrógeno. Em ratos, o tratamento com esteróides anabolizantes altera a metabolização periférica dos hormônios tireóideos e também parece causar importante efeito proliferativo sobre as células tireóideas. Assim, o presente artigo visa rever os dados publicados acerca dos efeitos de doses suprafisiológicas de esteróides anabolizantes sobre a função tireóidea, reforçando o perigo que a utilização indiscriminada dessas drogas pode causar à saúde. ABSTRACT Abuse of Anabolic Steroids and Its Impact on Thyroid Function.The use of anabolic steroids to increase physical performance and for aesthetic ends has reached alarming indices in the last three decades. Besides the desired actions, several collateral effects have been described in the literature, such as the development of some types of cancer, ginecomasty, peliosis hepatis, renal insufficiency, virilization, amongst others. The most proeminent effect on human thyroid function is the reduction of thyroxine binding globulin (TBG), with consequent reductions of total serum T 3 and T 4 , depending however on the susceptibility of the drug to aromatization and subsequent transformation into estrogen. In rats, anabolic steroids also act in the peripheral metabolism of thyroid hormones and seem to exert an important proliferative effect on thyroid cells. Thus, the aim of the present paper is to review data on the effect of supraphysiological doses of anabolic steroids on thyroid function, showing the danger that indiscriminate use of these drugs can cause to health.

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Testosterone and estradiol differentially regulate TSH-induced thyrocyte proliferation in immature and adult rats

Cited by 34 publications

References 21 publications

Sex differences in hepatic regulation of cholesterol homeostasis

Sex differences in hepatic regulation of cholesterol homeostasis

Androgen-mediated improvement of body composition and muscle function involves a novel early transcriptional program including IGF1, mechano growth factor, and induction of β-catenin

Abuso de esteróides anabolizantes e seu impacto sobre a função tireóidea

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