Vitamin D in Polycystic Ovary Syndrome: Relationship to BMI and insulin sensitivity

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 532-553-Hyperandrogenic Disorders
Basic/Clinical
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-549
Anju Elizabeth Joham*1, Samantha Cassar2, Nigel Stepto2, Cheryce L Harrison3, Samantha Kate Hutchison3, Sanjeeva Ranasinha3 and Helena Jane Teede4
1Monash University, Clayton VIC, Australia, 2Victoria University, Australia, 3Monash University, Clayton VIC, Australia, 4Monash University, Clayton VIC, Australia
Background: Vitamin D is a fat soluble vitamin that has been correlated with insulin resistance (IR) [1] and obesity, which is in part due to adipose tissue sequestration. Weight loss has been shown to improve both IR and Vitamin D levels [2]; however relationships between adiposity, Vitamin D and IR are unclear. Polycystic Ovary Syndrome (PCOS) is an insulin resistant condition with IR independent of and exacerbated by obesity [3], providing a model to explore these relationships.

Objective: To explore the relationships between Vitamin D, IR and body mass index (BMI) in women with PCOS and weight-matched controls.

 Design: Cross-sectional study

 Setting: Tertiary medical centre

 Participants: 21 overweight and 22 lean women with PCOS and 16 overweight and 19 lean BMI-matched control women without PCOS were studied at baseline.

 Method:  Following recruitment from community advertisement and screening, women were withdrawn from interfering medications and studied following a 3 month washout period. Blood samples were taken for Vitamin D and metabolic markers.  Detailed body composition measures and gold standard euglycaemic hyperinsulinaemic clamps were performed.

 Main Outcome Measures: Plasma levels of Vitmain D and glucose infusion rate (GIR) on clamp study and adiposity measures.

 Results: Vitamin D levels were not different between lean women with and without PCOS (49.8 and 49.5 nmol/L respectively, p=0.97). However, Vitamin D levels were lower in overweight PCOS women compared with overweight controls (31.6 and 46.1 nmol/L respectively, p=0.01). Overall correlations revealed strong correlation between GIR and BMI (r=-0.58) and moderate correlation with BMI (r=-0.34) and GIR (r=0.30). Independent regression analysis between Vitamin D and BMI revealed a beta coefficient of -0.86 (p=0.002), indicating for every 1 unit increase in BMI, Vitamin D is reduced by 0.86 nmol/L. For GIR and Vitamin D, the beta coefficient was 0.06, p=0.012.

 Sub-group analysis of the overweight cohort (n=37) showed that the PCOS group had significantly lower Vitamin D levels compared to the overweight non-PCOS group (beta coefficient -14.46, p=0.01). This difference in Vitamin D levels remained significant after adjusting for BMI (beta coefficient =-13.96, p=0.01). However, when adjusted for GIR this difference in Vitamin D was no longer significant between the two groups. Testing for effect modification on the Vitamin D and GIR relationship by PCOS status, adjusted for BMI, revealed that higher GIR levels were associated with higher Vitamin D levels for the non-PCOS group but this relationship was not evident for the PCOS cohort (beta coefficient (PCOS*GIR) -0.2, p=0.03).

 Conclusions: Vitamin D levels are lower in overweight women with PCOS compared to overweight controls but were similar within the lean cohort. Overall, BMI is the key correlate of Vitamin D status and this relationship may be in part mediated by IR.

1. Chiu KC, Chu A, Go VL, Saad MF. Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Am. J. Clin. Nutr. 2004;79(5):820-5. 2. Tzotzas T, Papadopoulou FG, Tziomalos K, Karras S, Gastaris K, Perros P, et al. Rising serum 25-hydroxy-vitamin D levels after weight loss in obese women correlate with improvement in insulin resistance. J Clin Endocrinol Metab 2010;95(9):4251-7. 3. Stepto NK, Cassar S, Joham AE, Hutchison SK, Harrison CL, Goldstein RF, et al. Women with polycystic ovary syndrome have intrinsic insulin resistance on euglycaemic-hyperinsulaemic clamp. Hum Reprod 2013.

Nothing to Disclose: AEJ, SC, NS, CLH, SKH, SR, HJT

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: This work was supported as an investigator initiated trial funded by a competitive grant from Monash University and Jean Hailes Foundation. Helena J Teede and Nigel K Stepto are supported by a research grant from the National Health and Medical Research Council of Australia (NHMRC) and Helena J Teede is also a NHMRC Research Fellow.