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The lower limits of quantifications are achieved at 250 pg/mL for DHEA, 200 pg/mL for 5-androstenediol (5-diol), 12 pg/mL for androstenedione (4-dione), 50 pg/mL for testosterone (Testo), 10 pg/mL for dihydrotestosterone (DHT), 4 pg/mL for estrone (E1) and 1 pg/mL for estradiol (E2). The linearity and accuracy of quality controls (QCs) and endogenous quality controls (EndoQCs) are according to the guidelines of the regulatory agencies for all seven compounds. testosterone.

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Although sex hormone-binding globulin (SHBG) and testosterone (T) have been inversely associated with risk of diabetes, few studies have examined dihydrotestosterone (DHT), a more potent androgen than T, in older adults, whose glycemic pathophysiology differs from younger adults. testosterone.

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Testosterone (T) synthesised in Leydig cells enters the epididymis and may there be converted into dihydrotestosterone (DHT) by 5α-reductase (5α-red) or into 17β-oestradiol (E2) by P450 aromatase (P450-aro). D-aspartate (D-Asp) is known to induce T synthesis in the testis. In this study, we investigated the effects of in vivo D-Asp administration in two major regions of the rat epididymis (Region I: initial segment, caput, corpus; Region II: cauda). The results suggest that exogenous D-Asp was taken up by both regions of rat epididymis. D-Asp administration induced a rapid increase in T, followed by a more gradual decrease in the T : DHT ratio in Region I. In Region II, T levels rapidly decreased and the T : DHT ratio was consistently lower relative to the control. Expression of 5α-red and androgen receptor genes showed a good correlation with DHT levels in both regions. D-Asp treatment also induced an increase of both E2 levels and oestradiol receptor-α (ERα) expression in Region I, whereas neither E2 levels nor ERα expression were affected in Region II. The early increase of P450-aro expression in Region I and late increase in Region II suggests a direct involvement of D-Asp modulation in P450-aro gene expression. Our results suggest that D-Asp modulates androgen and oestrogen levels and expression of androgen and oestrogen receptors in the rat epididymis by acting on the expression of 5α-red and P450-aro genes. testosterone.

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In boys and adolescents with monorchidism, there is a dissociated capacity of the remaining testis to compensate for the absence of the other gonad: while Leydig cell function is largely compensated, Sertoli cell proliferation and function was lower than in controls. testosterone.

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It has been speculated that testosterone stimulates erythropoiesis. We hypothesized that hemoglobin levels in hemodialysis (HD) patients are associated with serum testosterone concentrations. Testosterone, hemoglobin, and other biochemical parameters were measured in a representative sample of 98 chronic HD patients (50 male, 48 female; age 30-90 years, mean 65±13.9 years). We investigated relations among serum testosterone concentration, hemoglobin, ferritin, albumin, body mass index, lean body mass, total cholesterol, low-density lipoprotein and high-density lipoprotein cholesterol, triglycerides, high-sensitivity C-reactive protein (hsCRP), calcium (Ca), P, intact parathyroid hormone, N-terminal pro-brain natriuretic peptide, Karnofsky performance status, and blood pressure (BP) before and after HD. A statistically significant positive correlation between testosterone and hemoglobin was found in all patients (r=0.25, P<0.01), men (r=0.34, P<0.02), but not in women (r=0.27, P=0.07). Multiple regression analysis for all patients has shown statistically significant association between hemoglobin and testosterone (P<0.001), hsCRP (P<0.005), lean body mass (P<0.05), post-HD systolic (P<0.04), and diastolic BP (P<0.005). Multiple regression analysis in men has shown an association between hemoglobin and testosterone (P<0.04) and post-HD diastolic BP (P<0.04) and in women association between hemoglobin and testosterone (P<0.04), Ca (P<0.03), and post-HD diastolic BP (P<0.03). We found an association between serum testosterone concentration and hemoglobin in male and female HD patients. testosterone.

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A total of 366 (22.4%) and 417 (25.5%) women had mild and moderate-severe hepatic steatosis, respectively. FSH was negatively correlated with waist circumference, homeostasis model assessment of insulin resistance (HOMA-IR), and other metabolic factors (all P < 0.05). After adjusting for age, estradiol, and total testosterone, increased quartiles of FSH were associated with significantly decreased odds ratios of mild and moderate-severe groups (both P for trends <0.05). After further adjustment for waist circumference and HOMA-IR, FSH was no longer associated with mild hepatic steatosis. The association of FSH with moderate-severe hepatic steatosis was attenuated by waist circumference and HOMA-IR but persisted in the fully adjusted model (P for trend <0.01). testosterone.

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