Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 P535

ECE2010 Poster Presentations Male reproduction (28 abstracts)

Testosterone partially ameliorates metabolic profile and erectile responsiveness to PDE5 inhibitors in an animal model of male metabolic syndrome

Linda Vignozzi 1 , Sandra Filippi 2 , Annamaria Morelli 1 , Aravinda K Chavalmane 1 , Erica Sarchielli 3 , Gabriella B Vannelli 3 , Edoardo Mannucci 4 & Mario Maggi 1

1Sexual Medicine and Andrology Unit, University of Florence, Florence, Italy; 2Interdepartmental Laboratory of Functional and Cellular Pharmacology of Reproduction, University of Florence, Florence, Italy; 3Department of Anatomy, Histology and Forensic Medicine, University of Florence, Florence, Italy; 4Diabetes Section Geriatric Unit, Department of Critical Care, Florence, Italy.

Metabolic syndrome (MetS) is a clustering of cardio-metabolic risk factors (hyperglycemia, hypertension, dyslipidemia, visceral fat accumulation) that is also associated with hypogonadism and erectile dysfunction (ED). The study was aimed at clarifying the relationships among MetS, hypogonadism, and ED, we developed an animal model of MetS.

Methods: Male rabbits fed a high-fat diet (HFD), with or without testosterone (T) supplementation, were compared with control rabbits (fed a standard chow) and with rabbits made hypogonadal by a single injection of a long-acting GnRH-analog, triptorelin.

Main outcome measures: Evaluation of metabolic disturbances (plasma glucose, cholesterol, triglycerides, testosterone, LH, FSH level, glucose tolerance, mean arterial pressure, visceral fat accumulation), and corpora cavernosa (CC) relaxant capacity (in vitro contractility study) in HFD animals as compared with control, GnRH analog-treated rabbits, and T-supplemented HFD rabbits.

Results: HFD rabbits showed all the features of MetS. HFD induced hypogonadotropic hypogonadism is characterized by a reduction of plasma T, FSH, LH levels, testis and seminal vesicles weight, and testicular steroidogenic enzymes. Such a phenotype is similar to that induced by triptorelin administration. A reduced GnRH immunopositivity in hypothalamus suggests a central origin of HFD-related hypogonadism. HFD also induced penile alterations, as demonstrated by a reduction of acetylcholine-and electrical field stimulation-induced CC relaxation, hyper-responsiveness to the NO donor, SNP, and unresponsiveness to PDE5 inhibitors. Similar penile alterations were observed in triptorelin treated rabbit. In HFD, as well as in triptorelin treated rabbits, PDE5 and eNOS mRNA expression quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) were significantly decreased. T administration prevented almost all penile alterations observed in HFD rabbits. T treatment dramatically reduced HFD-induced visceral obesity, partially ameliorating also the metabolic profile.

Conclusion: We have developed an animal model of MetS associated with hypogonadotropic hypogonadism and penile alterations including unresponsiveness to PDE5 inhibitors. T supplementation was able to partially revert HFD-induced phenotype.

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