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Resistance exercise did not increase muscle concentrations of Testosterone in men or women.  The individuals in this study were actively training.  These were not sedentary individuals.

Great read on the regulation of the androgen receptor by the different iso forms of 5-alpha reductase and HSD.

inhibition of 11beta-HSD1 improves metabolic syndrome and atherosclerosis.  This suggests that metabolic syndrome is associated with increase 11beta-HSD1 expression/activity.  Animal study

Study proposes that 11beta-HSD type 1 is the key to linking glucocorticoids and metabolic dysfunction.  The key point of this study is that it is the adipose tissue expression of 11beta-HSD type 1 that is the key.

another nice article on the dysregulation of cortisol and its role in insulin resistance, metabolic syndrome, and obesity.

Peripheral 11Beta-HSD1 plays critical role in fat metabolism and energy utilization.  Good discussion on the role that extra-adrenal 11Beta-HSD1 plays in metabolism

DHT metabolites play an important role of intra-prostate DHT synthesis in those following ADT.  This is a proposed mechanism for the failure rate and aggressive nature of prostate cancer that fails ADT.   3-alpha androstanediol is converted via 3 alpha HSD back to DHT.  In contrast, 3-beta androstanediol cannot.

good review of 11beta-HSD type 1 activity.

impaired cortisone to cortisol found in obese individuals.  This occurred through a decrease in 11beta-HSD type 1 activity.

adipocytes increase genetic expression of 11beta-HSD. This increases local cortisol production from cortisone.  This plays a pivotal role in obesity.  Question:  would this play a role in peripheral hypothyroid?  I think so.

Great article!!  Nice discussion of the complexity of hormones.  Women on aromatase inhibitors can make estrogen from Testosterone.  This is important with estrogen sensitive cancer as in breast cancer.  This will occur via alternative pathways: Testosterone to DHT via 5 alpha reductase and then DHT to 3 beta androstanediol via 3 beta HSD.  3 beta androstanediol is a male hormone metabolite that binds to estrogen receptors.  The affinity is less than Estradiol, but appears to have a higher affinity for ER beta over ER alpha. 

Animal study, finds that DHEA inhibited 11beta-HSD type I and thus improved glucose uptake and adipocyte proliferation.  This effect occurred peripherally.

Article finds that carbohydrate meals cause increase in extra-adrenal cortisol more than protein and fat.  This is via 11beta-HSD1.

Increased visceral adiposity results in increased 11beta-HSD that results in increased cortisone to cortisol production preference.  Cortisol production doesn't just come from the adrenals--it is also produced and metabolized in peripheral and visceral fat.

acute stress is associated with increased 11beta-HSD2 in pregnant rat model.

11beta-HSD type I and type II are no equally expressed across all tissues.  Endocrine disrupting chemicals (EDC) inhibit both.

hyperactive HPA axis associated with depression. This is becoming evident in the literature.  This study looked at SNPS in the etiology of elevated cortisol and/or androstenedione.  They followed the results with saliva and found that 3 SNPS were associated with increased 11Beta-HSD1 activity and associated increased depression.

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.

obesity is associated with increased cortisol metabolism.  This would be found in increased urinary metabolites, especially via the 5-allpha reductase pathway.  Increased cortisone to cortisol production occurs via 11 beta-HSD1.  This occurs predominately in adipose tissue.  The thought here is cortisol metabolism is tissue specific and functionally different.

lean women with PCOS found to have reduced 11 beta-HSD1 and increased 5 alpha reductase activity.  This, in part, is associated with the elevated cortisol and androgens in these women.