The effects of vitamin D on the early pubertal onset and the gonadotropin-releasing hormone (GnRH) neuronal activities

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 624-646-Growth: Clinical Trials & Observational Studies
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-645
Min Sun Kim*1, Seong Kyu Han2 and Dae-Yeol Lee3
1Chonbuk Natl Univ Med Schl, Jeonju, South Korea, 2Department of Oral Physiology, School of Dentistry & Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea, Jeonju-si, South Korea, 3Chonbuk National University Medical School, Jeonju, South Korea
Purpose; Many reports have shown that vitamin D status is related to bone health, metabolic syndrome, autoimmune diseases, cancer and earlier menarche. In this study, we examined the association of serum 25-hydroxyvitamin D (25OHD) levels with early pubertal onset and the effect of 25OHD on GnRH neuronal activities.

Methods; We included 110 girls aged 7 to 10 years during winter (normal puberty group, 75 girls; central precocious puberty group, 35 girls). Pubertal development was assessed by Tanner staging and central precocious puberty (CPP) was diagnosed by clinical characteristics with GnRH stimulation test. They were subdivided according to serum 25OHD levels (severe deficiency, <10 ng/mL; deficiency, <20 ng/mL; insufficiency, 20-29 ng/mL; sufficiency, ≥30 ng/mL). In this study, following laboratory tests were included: fasting lipid profile (cholesterol, triglyceride and LDL), serum alkaline phosphatase (ALP), calcium, phosphorus and 25OHD. In addition, conventional whole cell voltage clamp technique was used to investigate the effects of 25OHD on N-methyl-D-aspartate (NMDA)-mediated response on GnRH neurons.


1)      Serum 25OHD levels in girls with CPP were found to be lower than in girls with normal puberty (13.28±4.04 vs 11.29±3.77 ng/mL, p<0.05) and prevalence of severe vitamin D deficiency was significantly higher in CPP group than that of normal group (21.3 vs 44.1 %, p<0.05).

2)      There were no significant differences in age, BMI, serum ALP, LH, estradiol and lipid profiles between CPP and normal puberty group. However, serum 25OHD levels were significantly negatively associated with serum ALP levels.

3)      NMDA (30 uM) was applied on GnRH neurons in the presence and absence of vitamin D (OHD, 10 nM). All juvenile neurons tested were responded to the applied NMDA and the NMDA-mediated responses were affected by pre-application of OHD. NMDA in the presence of OHD showed the decrease in the frequency of postsynaptic currents in 5 GnRH neurons tested (NMDA, 5.13 ± 1.02 Hz; OHD+NMDA, 3.08 ± 0.61 Hz, p<0.05). Furthermore, the holding current changed by NMDA application was decreased in the presence of OHD and recovered after washout (NMDA,-44.18±5.59 pA ; OHD +NMDA, -19.36 ± 6.17 pA, washout, -34.08 ± 4.38, n=5 pA, p<0.05).


Conclusion; We found that serum 25OHD levels were significantly lower in girls of CPP with high prevalence of vitamin D deficiency than in normal puberty girls. In addition, exogenous vitamin D suppressed NMDA-mediated GnRH neuronal excitation. These findings suggest that vitamin D may inhibit early pubertal onset and/or rapid progression of puberty, at least in part, through suppression of NMDA-mediated GnRH neuronal excitation in human. Further studies including animal study are necessary in order to clarify this association.

Nothing to Disclose: MSK, SKH, DYL

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