ECE2015 Oral Communications Reproduction (5 abstracts)
Decanoic acid inhibits androgen production in vitro and in vivo by regulating HSD3B2: a promising drug candidate for the management of hyperandrogenism in polycystic ovary syndrome
Bao Hui Lee 1, , Huey Min Tan 1 , Yu Li 1 , Zhiwei Zhang 1 , Inthrani Raja Indran 1 , Jun Li 1 & Eu Leong Yong 1
1National University of Singapore, Obstetrics & Gynaecology, Singapore, Singapore; 2National University of Singapore, NUS Graduate School for Integrative Sciences & Engineering, Singapore, Singapore.
Background: Polycystic Ovary Syndrome (PCOS) is an endocrine disorder characterized by hyperandrogenism in women, with a high incidence of insulin resistance. Decanoic acid (DA), a naturally occurring 10-carbon fatty acid, has been shown to improve insulin sensitivity and lipid profile in an in vivo model of diabetes without the induction of weight gain. However, the effects of DA on androgen production has not been explored.
Aim: The objective of this study was to evaluate the effects of DA on androgen production and regulation of steroidogenic enzymes in vitroand in vivo.
Methods: NCI-H295R human adrenocortical cells were used to assess the effects of DA on androgen production, gene and protein expression of the steroidogenic enzymes. In addition, an in vivo letrozole-induced PCOS rat model was used to assess if oral administration of glyceryl tridecanoate (GT), the triglyceride form of DA, may restore normal androgen production and alleviate the symptoms associated with PCOS.
Results: Our findings demonstrate that DA significantly inhibits gene and protein expression of HSD3B2, and androgen production in NCI-H295R cells in a dose-dependent manner. Notably, oral feed of the letrozole-induced PCOS rats with GT restored estrous cyclicity, reduced serum testosterone, and lowered fasting insulin.
Conclusion: Put together, this study has identified a natural compound, DA, as a promising drug candidate for the modulation of androgen biosynthesis. The inhibition of androgen biosynthesis by DA occurs, at least in part, via the suppression of HSD3B2, which codes for an essential enzyme in the steroidogenesis pathway. These results lay the platform for the development of DA for the management of hyperandrogenism and insulin resistance in PCOS.
Disclosure: This study was supported by a grant from the Singapore National Medical Research Council (NMRC/BnB/0007c/2013).
Volume 37
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Endocrine Abstracts
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