Testosterone and obesity in men under the age of 40 years

Гончаров, Н. П.; Katsya, G.V.; Chagina, N. A.; Gooren, Louis

doi:10.1111/j.1439-0272.2008.00863.x

Cited by 30 publications

(32 citation statements)

References 25 publications

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“…After 3 wk of treatment, serum total and free testosterone concentrations increased (P Ͻ 0.05) by approximately sevenfold (Table 1), toward the high end of the range for women with hyperandrogenemia/PCOS (41,49), but still below the normal range for eugonadal men (13). Plasma estradiol, progesterone, insulin and glucose concentrations, and the homeostasis model assessment of insulin resistance score were not affected by testosterone treatment (Table 1).…”

Section: Body Weight and Body Compositionmentioning

confidence: 93%

Testosterone increases the muscle protein synthesis rate but does not affect very-low-density lipoprotein metabolism in obese premenopausal women

Wang

Smith

Patterson

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Wang X, Smith GI, Patterson BW, Reeds DN, Kampelman J, Magkos F, Mittendorfer B. Testosterone increases the muscle protein synthesis rate but does not affect very-low-density lipoprotein metabolism in obese premenopausal women. Am J Physiol Endocrinol Metab 302: E740 -E746, 2012. First published January 17, 2012; doi:10.1152/ajpendo.00533.2011.-Men and women with hyperandrogenemia have a more proatherogenic plasma lipid profile [e.g., greater triglyceride (TG) and total and low-density lipoprotein-cholesterol and lower high-density lipoprotein-cholesterol concentrations] than healthy premenopausal women. Furthermore, castration of male rats markedly reduces testosterone availability below normal and decreases plasma TG concentration, and testosterone replacement reverses this effect. Testosterone is, therefore, thought to be an important regulator of plasma lipid homeostasis. However, little is known about the effect of testosterone on plasma TG concentration and kinetics. Furthermore, testosterone is a potent skeletal muscle protein anabolic agent in men, but its effect on muscle protein turnover in women is unknown. We measured plasma lipid concentrations, hepatic very low density lipoprotein (VLDL)-TG and VLDLapolipoprotein B-100 secretion rates, and the muscle protein fractional synthesis rate in 10 obese women before and after trandermal testosterone (1.25 g of 1% AndroGel daily) treatment for 3 wk. Serum total and free testosterone concentrations increased (P Ͻ 0.05) by approximately sevenfold in response to testosterone treatment, reaching concentrations that are comparable to those in women with hyperandrogenemia, but lower than the normal range for eugonadal men. Except for a small (ϳ10%) decrease in plasma high-density lipoprotein particle and cholesterol concentrations (P Ͻ 0.04), testosterone therapy had no effect on plasma lipid concentrations, lipoprotein particle sizes, and hepatic VLDL-TG and VLDL-apolipoprotein B-100 secretion rates (all P Ͼ 0.05); the muscle protein fractional synthesis rate, however, increased by ϳ45% (P Ͻ 0.001). We conclude that testosterone is a potent skeletal muscle protein anabolic agent, but not an important regulator of plasma lipid homeostasis in obese women. triglyceride; apolipoprotein B; muscle protein synthesis MEN HAVE A MORE PROATHEROGENIC plasma lipid profile, including greater plasma triglyceride (TG) and total and low-density lipoprotein (LDL)-cholesterol concentrations, lower high-density lipoprotein (HDL)-cholesterol concentration, and smaller HDL particles, than women (24, 25). Sex differences in the plasma lipid profile have traditionally been attributed to differences in the sex hormone milieu; particularly the availability of estradiol, but also progesterone. However, we and others have shown that changes in ovarian steroid concentration during the normal menstrual cycle (26) and after menopause (6, 23, 50) are not associated with changes in very-low-density lipoprotein (VLDL)-TG and VLDL-apolipoprotein B-100 (apoB-100) kinetics and concentrations that ...

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Section: Body Weight and Body Compositionmentioning

confidence: 93%

Testosterone increases the muscle protein synthesis rate but does not affect very-low-density lipoprotein metabolism in obese premenopausal women

Wang

Smith

Patterson

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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“…Indeed, male hormone levels diminish as the body mass index (BMI) increases, 14 an association affected by leptin both in male and female subjects. 15,16 Subfertility has been directly associated with CLGI and low testosterone levels. 17 In a cross-sectional study, CLGI, as demonstrated by elevated levels of the pro-inflammatory cytokine TNFa and the chemokines MIP1a and MIP1b, was associated with low testosterone and subfertility regardless of BMI.…”

Section: Effects Of Metabolic Inflammation On the Hpg Axismentioning

confidence: 99%

The impact of adipose tissue-derived factors on the hypothalamic-pituitary-gonadal (HPG) axis

et al. 2015

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Adipose tissue produces factors, including adipokines, cytokines and chemokines which, when released, systemically exert endocrine effects on multiple tissues thereby affecting their physiology. Adipokines also affect the hypothalamic-pituitary-gonadal (HPG) axis both centrally, at the hypothalamic-pituitary level, and peripherally acting on the gonads themselves. Among the adipokines, leptin, adiponectin, resistin, chemerin and the peptide kisspeptin have pleiotropic actions on the HPG axis affecting male and female fertility. Furthermore, adipokines and adipose tissue-produced factors readily affect the immune system resulting in inflammation, which in turn impact the HPG axis, thus evidencing a link between metabolic inflammation and fertility. In this review we provide an overview of the existing extensive bibliography on the crosstalk between adipose tissue-derived factors and the HPG axis, with particular focus on the impact of obesity and the metabolic syndrome on gonadal function and fertility.

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“…Serum testosterone levels are generally depressed in obese individuals [108,110]. This observation is likely due in part to increased conversion of androgens to estrogen via aromatase activity within the adipocytes.…”

Section: Molecular Mechanisms Of Obesity and Prostate Cancer Riskmentioning

confidence: 96%

Molecular Mechanisms of Obesity, Inflammation and Cancer: The Use of in vitro Model Approaches for Targeted Prevention Strategies

Fenton¹,

McCaskey²,

Woodworth³

2010

TOOBESJ

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Hormones, growth factors and cytokines produced by adipocytes are associated with cancer progression. We suggest that chronically elevated adipokines as observed in the obese state may have profound effects locally on colon epithelial cells through growth promotion effects, induction of autocrine signaling, angiogenesis and immune cross-talk. This dysregulation of the local environment via a systemic signal may lead to the promotion of colon cancer via a novel set of mechanisms. Elucidating the mechanisms by which obesity may increase cancer risk may lead to the identification of treatment/prevention targets. The use of models of this multistage process should allow for mechanism-based approaches to block phenotypes associated with the process of carcinogenesis. The review highlights using in vitro model systems of these various stages to understand the molecular mechanisms of obesity and cancer risk. The advantage in using these systems is that the response of cells possessing various transformations can be compared to "normal cells". The key is to identify targets that are aberrant from normal to perturb for cancer prevention strategies. This approach would theoretically reduce the possibility of severe or unwanted side-effects when the target does not also destroy the normal cell mechanisms. Cell models can aid in the identification of those targets and inform rationale translation to animal and human studies.

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Testosterone and obesity in men under the age of 40 years

Cited by 30 publications

References 25 publications

Testosterone increases the muscle protein synthesis rate but does not affect very-low-density lipoprotein metabolism in obese premenopausal women

Testosterone increases the muscle protein synthesis rate but does not affect very-low-density lipoprotein metabolism in obese premenopausal women

The impact of adipose tissue-derived factors on the hypothalamic-pituitary-gonadal (HPG) axis

Molecular Mechanisms of Obesity, Inflammation and Cancer: The Use of in vitro Model Approaches for Targeted Prevention Strategies

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