Biomedical subjects

C Pelusi

Publications and source records attributed to C Pelusi.

5 recordsLinked to original sources

PubMed2005

Short-term modification of sex hormones is associated with changes in ghrelin circulating levels in healthy normal-weight men.

The aim of this study was to evaluate the effect of selective and short-term sex hormone modifications on ghrelin levels in normal-weight eugonadal men undergoing hormonal contraceptive treatments. Seven men received an oral progestin [cyproterone acetate (CPA) or dienogest (DNG)] 10 mg/day for 3 weeks (CPA-DNG group), 7 CPA orally 5 mg/day in association with testosterone enanthate (TE) im 200 mg/week for 8 weeks (CPA-TE group), and 7 placebo (PLAC) for 8 weeks (PLAC group). Anthropometry and blood levels of LH, FSH, testosterone, estradiol, glucose, insulin and total ghrelin were evaluated. At baseline, no parameters differed among the three groups. After treatment, LH and FSH decreased in both CPA-DNG and CPA-TE groups, whereas they did not change in the PLAC group. Testosterone and estradiol decreased in the CPA-DNG group to the hypogonadal range, increased in the CPA-TE group to supraphysiological concentrations and, as expected, remained unchanged in the PLAC group. Total ghrelin levels increased in the CPA-DNG, decreased in the CPA-TE and did not change in the PLAC group. Ns modifications in the other parameters were observed in any group, demonstrating that the short-term changes of circulating sex hormones are able to modify ghrelin levels. These data, therefore, suggest that sex steroids are important regulators of ghrelin in normal-weight healthy men too.

Adult↗

PubMed2003

Testosterone levels in obese male patients with obstructive sleep apnea syndrome: relation to oxygen desaturation, body weight, fat distribution and the metabolic parameters.

To investigate the impact of obstructive sleep apnea syndrome (OSAS) on testosterone levels and on the main parameters of the metabolic syndrome in abdominally obese men, 15 male subjects with abdominal obesity phenotype and polysomnographic diagnosis of OSAS (OB-OSAS) and 15 controls matched for age and anthropometric parameters (OB) were investigated. Anthropometry, SHBG, sex hormones and several parameters of the metabolic syndrome were measured. Only subjects with an Epworth Sleepiness Score greater than 10 underwent a polysomnographic study with calculation of the number of desaturation rates per sleeping hour (ODI), the minimal oxygen saturation during each desaturation episode (minSaO2) and the mean minimal arterial oxygen saturation for the whole night period (MminSaO2). Both total and free testosterone levels were lower in OB-OSAS than in OB patients. A negative correlation between polysomnographic parameters (ODI, minSaO2 and MminSaO2) and testosterone levels was found. The relationship between total and free testosterone and ODI persisted after adjusting for body mass index (BMI) and waist (W) values. Triglyceride and uric acid levels were significantly higher in OB-OSAS than in OB patients. A negative correlation between testosterone and acid uric level and a positive correlation between testosterone and HDL-cholesterol level was found, regardless of BMI and W circumference, particularly in the OB-OSAS group. Our study suggests that, in patients with obesity and OSAS, the severity of hypoxia during sleeping hours may be an additional factor in reducing testosterone levels, regardless of BMI and abdominal fatness. This may contribute in worsening metabolic abnormalities which, in men with OSAS, exceed those expected on the basis of degree of obesity and pattern of fat distribution.

Adipose Tissue↗

PubMed2003

Testosterone undecanoate maintains spermatogenic suppression induced by cyproterone acetate plus testosterone undecanoate in normal men.

In this study we evaluated whether testosterone undecanoate (TU), alone or combined with low dose cyproterone acetate (CPA), can maintain spermatogenic suppression induced by higher doses of CPA plus TU. Twenty-four men received for 12 wk 20 mg/d CPA plus 1000 mg/6 wk TU and then 1000 mg/8 wk TU plus 20 mg/d CPA (n = 8), 2 mg/d CPA (n = 8), or plus placebo (n = 8) for 32 wk. Blood samples, physical examinations, hormones, chemistry, hematology, semen analysis, and sexual/behavioral assessments were performed throughout the study. Sperm counts decreased to less than 1 million/ml in all subjects by wk 12, and 54% of them achieved azoospermia. Suppression of sperm counts was maintained until wk 44. Serum LH and FSH levels were suppressed by wk 12 of hormone administration and remained suppressed until wk 44. No significant changes in any biochemical parameters were detected at wk 44 in any group. There was a slight increase in total prostate volume to within the normal range at wk 44 that returned to baseline 1 yr after stopping hormone administration. In conclusion, TU alone or combined with lower doses of CPA maintains sperm suppression induced by higher dose CPA plus TU for 32 wk. This prototype regimen represents a promising male contraceptive regimen.

Adult↗

PubMed2002

Obesity and the polycystic ovary syndrome.

The polycystic ovary syndrome (PCOS) is a condition characterized by hyperandrogenism and chronic oligo-anovulation. However, many features of the metabolic syndrome are inconsistently present in the majority of women with PCOS. Approximately 50% of PCOS women are overweight or obese and most of them have the abdominal phenotype. Obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and an increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinemia in women with PCOS. Therefore, obesity-related hyperinsulinemia may play a key role in favouring hyperandrogenism in these women. Other factors such as increased estrogen production rate, increased activity of the opioid system and of the hypothalamic-pituitary-adrenal axis, decreased sex hormone binding globulin synthesis and, possibly, high dietary lipid intake, may be additional mechanisms by which obesity favours the development of hyperandrogenism in PCOS. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCOS women. This picture tends to be more pronounced in obese PCOS women with the abdominal phenotype. Body weight loss is associated with beneficial effects on hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding insulin-sensitizing agents and/or antiandrogens to weight reduction programmes. These obviously emphasize the role of obesity in the pathophysiology of PCOS.

Androgens↗

PubMed2001

Testosterone in ageing men.

A progressive decline in androgen levels is a common finding in men after middle age. The resulting clinical picture may be characterised by alterations in the physical and psychological domains, which have been demonstrated to correlate positively with testosterone serum levels. This clinical picture closely resembles the features of primary or secondary hypogonadism. Testosterone is the more convenient hormone for substitution therapy in classic hypogonadism as well as in age-related hypoandrogenism. Different choices of testosterone preparations are currently available, which are characterised by different routes of administration and by various pharmacokinetic profiles. Two major achievements urgently need to be investigated in the near future: the ability of the new formulations to reach more physiological and sustained hormone levels with the concomitant amelioration of their tolerability and the evidence of long-term prospective studies aimed at demonstrating the benefits and the possible complications of this therapy.

Aged↗