Posts Tagged ‘Free Testosterone’

Dermal Papilla Androgen Sensitivity, Androgen Receptors & Methylation

Thursday, December 30th, 2010

Due to the understanding of male pattern baldness as Androgenic Alopecia (i.e. as an androgen-dependent process), many studies have focused on androgen metabolism (AM) in the body and how androgens effect hair.  Studies have shown that “all dermal papilla cells from androgen-sensitive sites contain low capacity, high affinity androgen receptors.” [18]

The dermal papilla (DP), at the base of the hair follicle, has androgen receptors (AR’s) that androgens from the blood bind to. In androgen-sensitive follicles, the androgens are synthesized and diffused over small distances; this induces changes in neighboring cells (like keratinocytes cells) in what is known as “paracrine interactions”. The diffusible proteins are called paracrine factors. [18]

When beard and scalp cells were incubated in androgens, androgens stimulated the cells’ ability to triggered mitosis (cell division) in beard cells but not in scalp cells. The interesting outcome here was that incubation with androgens had the exact opposite effect on scalp cells; these (scalp) cells’ mitogenic capacity was inhibited. [18]

Androgen-sensitive follicles are not simply targeted and affected by androgens; they are actually involved in androgen metabolism (AM) and can convert androgens using steroid-producing (steroidogenic) enzymes, also known as intrafollicular steroidogenic enzymes. [25]

A 2004 study shed more light on specific processes that shorten the hair cycle (that occur within the DP). According to the study, the three processes are as follows: “(1) the conversion of testosterone to DHT by type II 5-alpha-reductase; (2) the synthesis of TGF-beta2 in dermal papilla cells; and (3) the activation of the intrinsic caspase network.” [6]

The research seems to indicate AM activity at the DP of the hair follicle, amongst other interactions is not fully understood yet. Some of the known intrafollicular steroidogenic enzymes found in the DP are: Steroid Sulfatase (STS), 17beta-hydroxysteroid dehydrogenases (17b-HSD), 3beta-hydroxysteroid dehydrogenases (3b-HSD)  and type 1 and 2 5alpha-reductase (type 1 and type 2 5alpha-R). Type 2 5-alpha-reductase has been the target of a number of studies that showed it to accelerate the conversion of free testosterone into DHT. [10] [11] [12] [24] [25] [28] [31]

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Free Testosterone

Thursday, December 30th, 2010

The levels of free testosterone (free T) and the type 2 5alpha-reductase enzyme in serum has been the target of research; there seems to exist a strong coloration between the levels of available free testosterone in serum of the human body and baldness. [21] [23]

A 1997 study found that “several strong associations also were found between hormone levels and hair patterning.” This study found that “men with vertex and frontal baldness had higher levels of free T”. [2]

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It is also known that both 5alpha-reductase enzymes types 1 and 2 convert testosterone (T) to dihydrotestosterone (DHT) as mentioned earlier, [4] particularly type 2.

Clin Endocrinol (Oxf). 2009 Oct;71(4):494-9. “Androgenetic alopecia and insulin resistance in young men”

Wednesday, August 18th, 2010

-::- Note: The below is published here for archival purposes -::-

Clin Endocrinol (Oxf). 2009 Oct;71(4):494-9.

Androgenetic alopecia and insulin resistance in young men.

González-González JG, Mancillas-Adame LG, Fernández-Reyes M, Gómez-Flores M, Lavalle-González FJ, Ocampo-Candiani J, Villarreal-Pérez JZ.

Servicio de Endocrinologia, Dr Jose Eleuterio Gonzalez University Hospital, Facultad de Medicina, Universidad Autonoma de Nuevo Leon, Ave. Madero y Gonzalitos S/N, Monterrey, Mexico. jgonzalezg@fm.uanl.mx

Abstract

BACKGROUND: Epidemiological studies have associated androgenetic alopecia (AGA) with severe young-age coronary artery disease and hypertension, and linked it to insulin resistance. We carried out a case-control study in age- and weight-matched young males to study the link between AGA and insulin resistance using the homeostasis model assessment of insulin resistance (HOMA-IR) index or metabolic syndrome clinical manifestations.

METHODS: Eighty young males, 18-35 years old, with AGA > or = stage III in the Hamilton-Norwood classification, and 80 weight- and age-matched controls were included. Alopecia, glucose, serum insulin, HOMA-IR index, lipid profile and androgen levels, as well as metabolic syndrome criteria, were evaluated.

RESULTS: The HOMA-IR index was significantly higher in cases than controls. Nonobese cases had a higher mean diastolic blood pressure and a more frequent family history of AGA than nonobese controls. A borderline difference in the HOMA-IR index was found in obese AGA cases vs. obese controls [P = 0.055, 95% confidence interval (CI) 2.36-4.20 vs. 1.75-2.73]. Free testosterone values were significantly higher in controls than cases, regardless of body mass index (BMI). A statistically significant additive effect for obesity plus alopecia was found, with significant trends for insulin, the HOMA-IR index, lipids and free testosterone when BMI and alopecia status were used to classify the participants.

CONCLUSIONS: Our results support the recommendation for assessing insulin resistance and cardiovascular-related features and disorders in all young males with stage III or higher AGA, according to the Hamilton-Norwood classification.

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