Group items tagged

IL‐6 increases PSA and androgen receptor expression through a STAT3‐dependent pathway in the absence of androgen in LNCaP cells. Our results agreed with those of an earlier study that indicated that IL‐6 induced expression of the androgen receptor, which up‐regulated PSA promoter activity in the androgen‐independent pathway. Moreover, curcumin blocked stimulation of IL‐6 on the androgen receptor, which attenuated PSA gene expression in a ligand‐independent manner.

Older study finds weak synthetic androgen improves weight loss in obese postmenopausal women.  This study compared nandrolone decanoate to spironolactone--an androgen receptor antagonist.  No change in glucose or insulin was seen.  Hard to draw a strong conclusion from this study due to the comparison of a synthetic androgen versus an anti-androgen.  This comparison could have exaggerated the benefit of androgen in these women.

this study found no increase in inflammatory cytokines in those men on androgen deprivation therapy for prostate cancer.  The question, is they evaluated testosterone in the serum, so did they really see a decrease in androgens or just a decrease in the transport of androgens.  Saliva would have detected a true androgen deficient state.

discussion of the declining levels of androgens in the aging male.  But the focus of this entire article is wrong.  They are focusing on the blood levels of these androgens.  The biological effects of hormones occur in tissue not blood.  Though this article provides a good discussion of how transport of androgens are effected, it falls far short of providing any useful clinical application, because it fails to discuss peripheral levels of androgens.  

In cases of CRPC, there is endogenous androgen synthesis from weaker adrenal androgens.  Also, the authors point to a unregulated AR sensitivity in the lower androgen environment created by ADT.

Study used saliva to measure Testosterone levels in men.  Testosterone levels were inversely associated with age, but positively associated with CAG repeat sequences in the AR.

Leptin appears to be a good marker of low Testosterone.  This study proposes that the mechanism of action is potentially 2 fold: first, a decrease in LH release by leptin (kisspeptin?) and 2nd, a directed decrease in Testosterone production by the leydig cells in the testes.

Many pesticides function as androgen receptor antagonists.  Others as Xenoestrogens.  Estrogen-like toxins and androgen receptor antagonists...a potent cocktail to disrupt male androgen signaling.

Awesome review on the current understanding of Testosterone and Diabetes, metabolic syndrome, and CVD.  This article even goes into the literature on androgen receptors.

great review of the current knowledge of how adipose tissue influences androgen production and how androgens influence adipose tissue.  For example, leptin has an androgen inhibition centrally and peripherally.

multi-center study finds no association between androgen receptor expression and invasive bladder cancer.  There was also no difference between male and female in androgen receptor expression.

Nice review of Testosterone levels and some of the evidence linking Diabetes with low T.  However, the conclusion by the authors regarding what is causing the low T in men with Diabetes is baffling.  The literature does not point to one cause, it is clearly multifactorial--obesity, inflammation, high aromatase activity...I would suggest the authors continue their readings in the manner.

Great review of androgen dependent and androgen independent prostate cancer.

androgen receptors play role in male infertility

good review of androgens and AR.

another awesome article dealing with hormone metabolites. Physicians that don't understand metabolites and receptors may be doing more harm than good.   One of the mainstays of the treatment of metastatic prostate disease is androgen deprivation therapy.  This article requires a reassessment of this due to the DHT metabolite 3-beta androstanediol.  This metabolite is produced from DHT production via the enzyme 3beta HSD.  This metabolite binds to ER beta, an estrogen receptor, and inhibits proliferation, migration, promotes adhesion (limits spreading), and stimulates apoptosis.  This is contrast to 3-alpha androstanediol.  Androgen deprivation therapy will decrease 3-beta androstanediol.  This is the likely reason for the increased aggressive prostate cancer found in those men using 5 alpha reductase inhibitors.

Androgen deprivation therapy reduces Telomerase activity in androgen dependent prostate cancer cell lines.  Conversely, Testosterone increases Telomerase activity.  In these cell lines Telomerase activity is positively associated with prostate cancer.

Nice review of the mixed data on Testosterone and Prostate disease. It is clear that Testosterone does not precipitate prostate cancer.  The intraprostatic hormone milieu likely is different than that present in the serum.  No surprise there.  5alpha reductase decreases prostate volume, PSA, and low-grade prostate cancer, but actually increases aggressive prostate cancer. Supraphysiologic doping in young men associated with no increase in prostate disease. PSA no longer to be followed in men < 55.  Mortality rate not changed.  PSA change of 1.4 ng/ml is appropriate for additional prostate evaluation.  Testosterone therapy on average increased 0.5 ng/ml. Still, no mention of aromatase activity in this article.  Why is it that hormone sensitive disease in men is only with regards to androgens and women estrogen.

to be read

This article discusses the failure of androgen deprivation therapy and prostate cancer.  This failure is quite common.  The authors point to alpha-DHT as the primary mechanism through AR stimulation.  However, we know that DHT metabolites also stimulate estrogen receptors.