Expression of leptin long-form receptor mRNA in luteinized granulosa cells of obese women with polycystic ovary syndrome

J Huazhong Univ Sci Technolog Med Sci. 2007 Aug;27(4):461-3. doi: 10.1007/s11596-007-0429-y.

Abstract

To investigate the expression of mRNA of leptin long-form receptor (OB-Rb) in luteinized granulosa cells of obese women with polycystic ovary syndrome (PCOS), and to determine the role of leptin in the physiopathology of PCOS, luteinized granulosa cells were collected from the follicle fluid of 10 obese women who met the diagnostic criteria for PCOS and their BMI was equal to or greater than 25 kg/m(2), and at the same time, granulosa cells were collected from 10 normal women undergoing IVF-ET who served as the control group. Some luteinized granulosa cells were taken from normal women for in-vitro culture, into which human leptin of different concentrations was added (0, 10, 100 and 1000 ng/mL). After stimulation with leptin for 48 h, RT-PCR was employed for the detection of the expression of OB-RLmRNA in the luteinized granulosa cells. Our results showed that the level of OB-RLmRNA in luteinized granulosa cells of obese PCOS women was higher than those in the control (P<0.05). In luteinized granulosa cells cultured in vitro and stimulated by human leptin for 48 h, the level of OB-RLmRNA was higher than those without leptin stimulation (P<0.01), and when leptin concentration was at 100 ng/mL, and the level of OB-R(L)mRNA reached a peak. It is concluded that in obese PCOS women, the level of serum leptin is increased, which promotes the expression of OB-R(L) in luteinized granulosa cells and increases the sensitivity of the granulosa cells to leptin. Leptin may contribute to anovulation in obese women with PCOS.

MeSH terms

  • Case-Control Studies
  • Female
  • Granulosa Cells / metabolism*
  • Humans
  • Luteinization
  • Obesity / complications
  • Obesity / metabolism*
  • Polycystic Ovary Syndrome / complications
  • Polycystic Ovary Syndrome / metabolism*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptors, Leptin / genetics
  • Receptors, Leptin / metabolism*

Substances

  • LEPR protein, human
  • RNA, Messenger
  • Receptors, Leptin