Horm Metab Res 2010; 42(10): 754-757
DOI: 10.1055/s-0030-1262837
Short Communication

© Georg Thieme Verlag KG Stuttgart · New York

Vitamin D Regulates Steroidogenesis and Insulin-like Growth Factor Binding Protein-1 (IGFBP-1) Production in Human Ovarian Cells

G. Parikh1 , M. Varadinova1 , P. Suwandhi1 , T. Araki1 , Z. Rosenwaks2 , L. Poretsky1 , D. Seto-Young1
  • 1G. J. Friedman Diabetes Institute and Division of Endocrinology, Department of Medicine, Beth Israel Medical Center, Albert Einstein College of Medicine, New York, USA
  • 2Center for Reproductive Medicine and Infertility, Weill Medical College of Cornell University, New York, USA
Further Information

Publication History

received 19.04.2010

accepted 12.07.2010

Publication Date:
13 August 2010 (online)

Abstract

Vitamin D Receptor (VDR) is expressed in both animal and human ovarian tissue, however, the role of vitamin D in human ovarian steroidogenesis is unknown. Cultured human ovarian cells were incubated in tissue culture medium supplemented with appropriate substrates, with or without 50 pM–150 pM or 50 nM−150 nM of 1,25-(OH)2D3, and in the presence or absence of insulin. Progesterone, testosterone, estrone, estradiol, and IGFBP-1 concentrations in conditioned tissue culture medium were measured. Vitamin D receptor was present in human ovarian cells. 1,25-(OH)2D3 stimulated progesterone production by 13% (p<0.001), estradiol production by 9% (p<0.02), and estrone production by 21% (p<0.002). Insulin and 1,25-(OH)2D3 acted synergistically to increase estradiol production by 60% (p<0.005). 1,25-(OH)2D3 alone stimulated IGFBP-1 production by 24% (p<0.001), however, in the presence of insulin, 1,25-(OH)2D3 enhanced insulin-induced inhibition of IGFBP-1 production by 13% (p<0.009). Vitamin D stimulates ovarian steroidogenesis and IGFBP-1 production in human ovarian cells likely acting via vitamin D receptor. Insulin and vitamin D synergistically stimulate estradiol production. Vitamin D also enhances inhibitory effect of insulin on IGFBP-1 production.

References

  • 1 Dukoh S, Donaldson CA, Marion SL, Pike JW, Haussler MR. Endocrinology. 1983;  112 200-206
  • 2 Yoshizawa T, Handa Y, Uematsu Y, Takeda S, Sekine K, Yoshihara Y, Kawakami T, Arioka K, Sato H, Uchiyama Y, Masushige S, Fukamizu A, Matsumoto T, Kato S. Nat Genet. 1997;  16 391-396
  • 3 Kinuta K, Tanaka H, Moriwake T, Aya K, Kato S, Seino Y. Endocrinology. 1999;  141 1317-1324
  • 4 Halloran BP, Deluca HF. J Nutr. 1980;  110 1573-1580
  • 5 Kwiencinski GG, Petrie GI, DeLuca HF. J Nutr. 1989;  119 741-744
  • 6 Agic A, Xu H, Altgassen C, Noack F, Wolfer M, Dierich K, Friedrich M, Taylor R, Hornung D. Reproductive Sciences. 2007;  14 486-497
  • 7 Seto-Young D, Zajac J, Liu H-C, Rosenwaks Z, Poretsky L. J Clin Endocrinol Metab. 2003;  88 3385-3391
  • 8 Seto-Young D, Leonardi O, Park A, Holcomb K, Salehi M, Chang P, Yih M, Rosenwaks Z, Poretsky L. Horm Res. 2003;  64 238-247
  • 9 Hodgins MB, Murad S. J Endocrinol. 1986;  110 R1-R4
  • 10 Teegarden D, Donkin SS. Nutrition Res Rev. 2009;  22 82-92

Correspondence

D. Seto-Young, PhD 

Division of Endocrinology

Beth Israel Medical Center

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