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.: Winstrol.. ajuda emagrecer? :.


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Visitante Sr.JoseBarriga

Ah tá...entao quer dizer que o uso dos aes nao ajuda na perda de gordura?

Nao sei pq mas eu acho que ajuda viu ...

Am J Physiol. 1998 Jun;274(6 Pt 1):C1645-52. Related Articles, Links

Androgen receptors in human preadipocytes and adipocytes: regional specificities and regulation by sex steroids.

Dieudonne MN, Pecquery R, Boumediene A, Leneveu MC, Giudicelli Y.

Service de Biochimie, Institut National de la Sante et de la Recherche Medicale CJF 9402, Faculte de Medecine Paris-Ouest, Universite Rene Descartes (Paris V), Centre Hospitalier de Poissy, 78303 Poissy Cedex, France.

Various clinical and epidemiological evidence strongly suggests a major role for sex steroid hormones in the determination of anatomical specificities of fat distribution in human. To date, no studies have examined the possible presence of androgen receptors (AR) in human adipocytes and preadipocytes. We have studied AR in preadipocytes from various anatomical locations (intra-abdominal and subcutaneous) in middle-aged men and women during the proliferation and differentiation processes (adipogenesis). Androgen binding sites quantified by [3H]R-1881-specific binding in whole cell extracts were twofold higher in intra-abdominal than in subcutaneous preadipocytes but identical for the same fat depots in men and women. Western blot analysis revealed 1) the presence of AR in the nuclear and cytosolic fractions of human preadipocytes, 2) a decrease of AR expression during adipogenesis, and 3) an upregulation of AR by androgens in vitro. RT-PCR experiments showed the presence of AR mRNA in human preadipocytes and adipocytes and also the regional specificity of AR distribution. However, AR mRNA expression was found to increase during adipogenesis. The same results were observed in rat preadipocytes. In conclusion, this study clearly demonstrates the presence of AR in human preadipocytes and adipocytes and suggests that androgens may contribute, through regulation of their own receptors, to the control of adipose tissue development.

PMID: 9611130 [PubMed - indexed for MEDLINE]

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Biochim Biophys Acta. 1995 May 11;1244(1):117-20. Related Articles, Links

Androgen hormone binding to adipose tissue in rats.

Sjogren J, Li M, Bjorntorp P.

Wallenberg Laboratory, Department of Heart and Lung Diseases, University of Goteborg, Sahlgren's Hospital, Sweden.

Nuclear binding of androgen was examined, using R 1881, a synthetic androgen. The amount of androgen-receptor complexes bound to isolated nuclei was determined in isolated adipocytes from the epididymal (Epi), retroperitoneal (Ret), inguinal (Ing) and mesenteric (Mes) adipose tissues from intact and castrated rats. The binding was specific and saturable with a Kd in the nanomolar range. Binding was examined after 2 days and after 1 and 2 weeks after castration, showing a higher binding in the Mes tissue in comparison with Ing at all time-points (P < 0.05). Mes adipocytes showed a trend (0.05 < P < 0.1) to up-regulate their binding capacity 2 days after castration, and a significant (P < 0.05) downregulation 2 weeks after castration. Two days after castration, R 1881 binding, expressed per mg triacylglycerol (TG), was generally higher in the Mes region (P < 0.05). This was not fully significant in comparison with Epi tissue in intact rats. When expressed per cell the differences were somewhat diminished, due to differences in cell sizes. Androgen binding showed a negative correlation with TG-uptake in vivo (r = 0.85, P < 0.01), suggesting that a higher density of androgen receptors leads to a more inhibited lipid uptake. In conclusion, a specific androgen receptor was demonstrated in adipose tissue in rat, showing regional differences and a negative correlation with the lipid accumulation of the tissue.

PMID: 7766646 [PubMed - indexed for MEDLINE]

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J Steroid Biochem Mol Biol. 1990 Nov 30;37(4):553-8. Related Articles, Links

Up-regulation of androgen receptor binding in male rat fat pad adipose precursor cells exposed to testosterone: study in a whole cell assay system.

De Pergola G, Xu XF, Yang SM, Giorgino R, Bjorntorp P.

Istituto di Clinica Medica, Universita di Bari.

Binding of androgens to adipocytes has previously been evaluated using cytosol fractions without taking into account nuclear binding, although the latter is suggested to be close to the physiological site of action. In the present study, performed in differentiated fat pad adipose precursor cells, we describe a simple, reliable and reproducible androgen binding assay in a system with intact cells. Tritiated and unlabeled methyltrienolone (R1881) were used to define specific and unspecific androgen binding. Triamcinolone acetonide was added to prevent the binding of R1881 to other types of receptors. Differentiated adipose precursor cells contain a homogeneous class of high affinity androgen binding sites, and binding is saturable and reversible. Binding apparently occurs at one site, with a Kd in the range of physiological androgen concentration (about 4 nM). Competition studies indicate that the receptor is specific for R1881, testosterone and dihydrotestosterone, which have approximately the same affinity, while progesterone, estradiol and dexamethasone show much lower affinity. Androgen binding was markedly enhanced after cellular exposure to R1881 and testosterone but not dihydrotestosterone, and this increase was dependent on protein synthesis, suggesting the formation of new receptors by these androgens. In conclusion, fully differentiated adipocytes contain a specific, high affinity receptor, the density of which is dependent on androgens.

PMID: 2278839 [PubMed - indexed for MEDLINE]

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Endocrinology. 1990 Feb;126(2):1229-34. Related Articles, Links

The effects of androgens on the regulation of lipolysis in adipose precursor cells.

Xu X, De Pergola G, Bjorntorp P.

Wallenberg Laboratory, Sahlgren's Hospital, University of Goteborg, Sweden.

Adipose precursor cells from male rats were exposed in primary culture to testosterone (T) or dihydrotestosterone (DHT), and their effects on the regulation of lipolysis were studied. T, but not DHT, stimulated catecholamine-induced lipolysis in a dose-dependent manner, including physiological concentrations. The effect was equally pronounced with isoproterenol (a pure beta-adrenergic agonist) and norepinephrine (a mixed alpha 2- and beta-adrenergic agonist). The higher lipolytic capacity of catecholamines on T-treated cells was paralleled by a similar increase in the number of beta-adrenoceptors in the cells, without a change in the receptor affinity, suggesting that T induced new synthesis or externalization of beta-adrenoceptors. Both T and DHT stimulated forskolin-induced lipolysis, suggesting an androgen effect at the level of the catalytic subunit of adenylate cyclase. The pertussis toxin-stimulated lipolysis was not influenced by the presence of androgens in the culture medium, and no effect was seen on the antilipolytic effect of insulin. These effects did not disappear in the presence of an aromatase inhibitor, suggesting that the T effects were not mediated by conversion to estrogens. These cells showed specific saturable binding for androgens, with a Kd in the range of androgen concentrations shown to be active. In conclusion, androgens enhance the lipolytic capacity of these cells by increasing the apparent number of beta-adrenoceptors (T only) and the activity of adenylate cyclase (both T and DHT). These changes are not mediated by conversion to estrogens. These effects probably occur via binding to specific androgen receptors.

PMID: 2153523 [PubMed - indexed for MEDLINE]

acho que nao né...?

deve ser tudo mentira....

e o homem tb nao foi pra lua, foi a globo que fez montagem

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Visitante Sr.JoseBarriga

ah sim havia me esquecido...vamos mostrar toda educaçao que ganhamos e vamos me aplaudir calorosamente...chame ai o papai, mamae, titio, amigos e conhecidos e todos vamos aplaudir!!

ps1: pq ao invez de usuario assiduo nao coloquem "o cara" para mim?

sem aquela piada q viu n muro escrito ....bla bla bla

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eu acho, e pelo conhecimento empirico (o de ver) que queima sim, mas nao de uma forma direta como um lipostabil ou termogenicos, mas com o aumento da sintese de proteina e com a troca de gordura por massa magra (como no treino normal)... ja vi muita gente que apos ciclo de winstrol ou nabolic strong que perde 2%, 3% de gordura.

obvio que quem tem 25, 30% de gordura no corpo, tomar com objetivo de perder 10kg, nao vai adiantar nada.

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  • 2 semanas depois...
gente.... peloamordedeus! a unica coisa q auxilia na queima de gordura sao os termogenicos

A unica coisa q podemos dizer eh q como os anabolizantes aumentam significativamente sua massa muscular (isso se vc treinar direito e fizer uma dieta condizente), seu gasto metabolico serah maior.... o q farah com q vc aumente sua qtidade de calorias proteinas e carbos por dia.

correção :: clenbuterol tb ajuda a perder gordura, e muitos ainda usam t3 pra queimar gordura...

fora isso o texto esta perfeito, excelente

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Visitante kusanagi

Porra Adriano é obvio que qualquer Ae aumenta a velocidade do metabolismo basal e isso por si só ja seria um potencial "fat burner" isso sem falar da capacidade de se ligar a alguns receptores das células de gordura e bla bla bla...

Nem é necessário tu postar esse texto.

Mas eh Phoda essa mulecada entender isso pq eles só usam pó de giz com áua achando que winstrol e óleo de girassol como deca Grega.

Por isso prefiro nem comentar esse tipo de coisa.

Mas já q tocou no assunto..

Vc sabe q está certo, mas pior q isso sabe q oq eu falei tbm eh verdade.

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Porra Adriano é obvio que qualquer Ae aumenta a velocidade do metabolismo basal e isso por si só ja seria um potencial "fat burner"

exatamente,a longo prazo tudo q faz ganhar massa irah fazer perder gordura,jah q irah aumentar o metabolismo,mas o sentido q estou faladno eh o mermo q o mestre ele naum irah farah perder "na hora".

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