Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 26 P350

ECE2011 Poster Presentations Steroid metabolism (10 abstracts)

Testosterone supplementation improves adipose tissue function in an animal model of metabolic syndrome

A Morelli 1 , E Maneschi 1 , L Vignozzi 1 , S Filippi 1 , M Marchetta 1 , B Mazzanti 1 , A Calcagno 2 , P Comeglio 1 , I Cellai 1 , G B Vannelli 1 & M Maggi 1


1University of Florence, Florence, Italy; 2University of Padoa, Padoa, Italy.


Introduction: Adipose tissue dysfunction is associated to metabolic syndrome (MetS), a clustering of cardio-metaboilic risk factors, including hypogonadism. We recently demonstrated that T supplementation was able to ameliorate the metabolic profile and reduce visceral fat accumulation in high-fat diet (HFD)-induced rabbit model of MetS.

Methods: We evaluated the differentiation capacity of preadipocytes (rPAD) obtained from visceral fat of the following rabbit groups: HFD (rPAD-HFD), T-supplemented HFD-rabbits (rPAD-T), standard diet (rPADcontrol) and HFD treated with INT-747 (rPAD-I), an agonist of the nuclear receptor FXR which previously showed the ability to reduce visceral fat accumulation in HFD-rabbits. rPAD were exposed to differentiating mixture (DIM) for 10 days and adipogenic potential was evaluated by quantitative analysis of trygliceride content and expression of adipocyte-specific genes.

Results: Histomorphometric analysis of visceral fat sections from all groups evidenced that adipocyte size was significantly increased in HFD-rabbit compared to control, indicating adipocyte dysfunction. Accordingly, rPAD-HFD showed a reduced capacity to accumulate triglyceride when exposed to DIM (84% over untreated cells) in comparison with rPADcontrol (318%). Moreover, glucose uptake in response to insulin was also reduced in rPAD-HFD. Interestingly, visceral adipocyte size was normalized in both T-and INT747-treated HFD rabbits. Functionally, rPAD-T and rPAD-I showed a triglyceride accumulation capacity after DIM (247 and 129%, respectively) and a glucose uptake ability comparable to that of rPADcontrol.

These findings were confirmed in terms of mRNA expression of adipocyte-specific genes (DKK1, FABP4, adiponectin and leptin), which were significantly induced in rPADcontrol, rPAD-T and rPAD-I, while remained unchanged in rPAD-HFD after exposure to DIM.

Conclusion: Overall, our results indicate that T-supplementation in the animal model of MetS may positively affect adipose tissue functions through the restoration of adipocyte commitment. This could reflect the ability of T in counteracting metabolic alterations most likely restoring adiponectin and insulin sensitivity in experimental MetS.

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