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Endocrine Abstracts (2012) 29 P491

Gifu University, Gifu, Japan.


Back ground: Numerous researches indicate that DHEA administration decreases fat mass in human and rodent. We evaluated the effects of DHEA treatment on adiposity. Male Otsuka Long evans fatty (OLETF) rats, hereditary obese type 2 diabetic animals derived from long evans tokushima (LETO) rats. These rats were fed with or without (control) 0.4% DHEA containing food for 52 weeks. Telomere length as a marker of whole cell division in adipose tissue were assessed. Genomic DNA isolated from fat tissue was digested with restriction enzyme, Hinf 1/Rsal, and then Southern analysis was performed to measure telomere length. Treatment with DHEA for 52 weeks in LETO and OLETF decreased fat mass. Furthermore, reduced telomere length in fat tissue isolated from OLETF and LETO rats was restored after treatment with DHEA. These results suggested that accelerated cell division in obese adipose tissue was prevented with DHEA administration.

Aim: We examined whether DHEA administration inhibited mature adipocyte proliferation in this study.

Methods: In vivo cell proliferation was estimated with 5′-bromo-2′-deoxyuridine (BrdU), a thymidine analog, uptake in adipose tissue. Male Wistar rats were fed with 0.4% DHEA or 0.005% pioglitazone, a thiazolidinedione, containing food for 4weeks, 200 mg/kg. BrdU was i.p. administered three times before sacrifice, then s.c., epididymal and periintestinal fats were collected. Immunohistochemical study using anti-BrdU antibody revealed that BrdU positive cells were identified both in stromal vascular fraction (SVF) and mature adipocyte.

Results: In visceral fat, BrdU positive cells were detected mainly in mature adipocyte. However they were observed predominantly in SVF area in subcutaneous fat. Treatment with DHEA mainly decreased BrdU positive cells in mature adipocyte. On the other hand, treatment with pioglitazone increased BrdU positive cells in SVF and mature adipocyte.

Conclusion: Considering the fact that DHEA reduce the expression of PPARg in adipocyte as reported previously, these results suggest that DHEA administration inhibited mature adipocyte proliferation, and PPARg may affect on mature adipocyte proliferation.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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