Adipocytes ESR1 Expression, Body Fat and Response to Testosterone Therapy in Hypogonadal Men Vary According to Estradiol Levels

madman

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In conclusion, all together, our results suggest the possibility that the persistently high E2 levels associated with obesity leads to ESR1 downregulation in adipocytes and reduced E2 sensitivity, which in turn results in attenuated fat mass loss in response to T therapy. Oestrogen resistance induced obesity was first described in a man with an inactivating mutation of the ESR1 [10]. Lack of E2 action predispose to metabolic syndrome, type 2 diabetes and cardiovascular events [6], conditions that affect both genders [8]. The identification of optimum serum E2 associated with the best E2 sensitivity and body composition profile is of clinical relevance, especially considering its influence on the response to hormone therapy as observed in our study. This is the first study showing: (1) the optimum E2 levels
associated with better body composition in HG men, (2) the existence of different E2 sensitivity based on circulating E2 and (3) its influence on the response to T therapy. Prospective investigations with a bigger sample size are needed to confirm our observation and to explore consequences of E2 resistance among individuals with hyperestrogenemia.
 

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Understanding Your Hormones

Estradiol (E2)

A form of estrogen produced from testosterone. Important for bone health, mood, and libido. Too high can cause side effects; too low can affect well-being.

DHT

Dihydrotestosterone is a potent androgen derived from testosterone. Affects hair growth, prostate health, and masculinization effects.

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The biologically active form of testosterone not bound to proteins. Directly available for cellular uptake and biological effects.

Scientific Reference

Lakshman KM, Kaplan B, Travison TG, Basaria S, Knapp PE, Singh AB, LaValley MP, Mazer NA, Bhasin S. The effects of injected testosterone dose and age on the conversion of testosterone to estradiol and dihydrotestosterone in young and older men. J Clin Endocrinol Metab. 2010 Aug;95(8):3955-64.

DOI: 10.1210/jc.2010-0102 | PMID: 20534765 | PMCID: PMC2913038

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