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Serum 25-Hydroxyvitamin D Levels, phosphoprotein enriched in diabetes gene product (PED/PEA-15) and leptin-to-adiponectin ratio in women with PCOS.

Savastano S, Valentino R, Di Somma C, Orio F, Pivonello C, Passaretti F, Brancato V, Formisano P, Colao A, Beguinot F, Tarantino G - Nutr Metab (Lond) (2011)

Bottom Line: Vitamin D is endowed with pleiotropic effects, including insulin resistance (IR) and apoptotic pathway.An inverse correlation was observed between 25(OH)D and BMI, PED/PEA-15 protein abundance, insulin, HoMA-IR, FAI (p < 0.001), and L/A (p < 0.05).Lower 25(OH)D and higher L/A were associated to PED/PEA-15 protein abundance in PCOS, suggesting their involvement in the ovarian imbalance between pro-and anti-apoptotic mechanisms, with high L/A and insulin and low 25(OH)D levels as the main determinants of PED/PEA-15 protein variability.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Molecular and Clinical Endocrinology and Oncology, Division of Endocrinology, University Federico II of Naples, Via S, Pansini 5, Naples, 80131, Italy. sisavast@unina.it.

ABSTRACT

Background: Polycystic ovary syndrome (PCOS) is frequently associated with hypovitaminosis D. Vitamin D is endowed with pleiotropic effects, including insulin resistance (IR) and apoptotic pathway. Disruption of the complex mechanism that regulated ovarian apoptosis has been reported in PCOS. Phosphoprotein enriched in diabetes gene product (PED/PEA-15), an anti-apoptotic protein involved in type 2 diabetes mellitus (T2DM), is overexpressed in PCOS women, independently of obesity. Leptin-to-adiponectin ratio (L/A) is a biomarker of IR and low-grade inflammation in PCOS. The aim of the study was to investigate the levels of 25-hydroxy vitamin D (25(OH)D), and L/A, in association with PED/PEA-15 protein abundance, in both lean and overweight/obese (o/o) women with PCOS.

Patients and methods: PED/PEA-15 protein abundance and circulating levels of 25(OH)D, L/A, sex hormone-binding globulin, and testosterone were evaluated in 90 untreated PCOS patients (25 ± 4 yrs; range 18-34) and 40 healthy controls age and BMI comparable, from the same geographical area. FAI (free androgen index) and the homeostasis model assessment of insulin resistance (HoMA-IR) index were calculated.

Results: In o/o PCOS, 25(OH)D levels were significantly lower, and L/A values were significantly higher than in lean PCOS (p < 0.001), while there were no differences in PED/PEA-15 protein abundance. An inverse correlation was observed between 25(OH)D and BMI, PED/PEA-15 protein abundance, insulin, HoMA-IR, FAI (p < 0.001), and L/A (p < 0.05). At the multivariate analysis, in o/o PCOS L/A, insulin and 25(OH)D were the major determinant of PED/PEA-15 protein abundance (β = 0.45, β = 0.41, and β = -0.25, respectively).

Conclusions: Lower 25(OH)D and higher L/A were associated to PED/PEA-15 protein abundance in PCOS, suggesting their involvement in the ovarian imbalance between pro-and anti-apoptotic mechanisms, with high L/A and insulin and low 25(OH)D levels as the main determinants of PED/PEA-15 protein variability. Further studies, involving also different apoptotic pathways or inflammatory cytokines and granulosa cells are mandatory to better define the possible bidirectional relationships between 25(OH)D, PED/PEA-15 protein abundance, leptin and adiponectin in PCOS pathogenesis.

No MeSH data available.


Related in: MedlinePlus

Correlations between variables in the study population. 25(OH)D, 25(OH) Vitamin D; BMI, body mass index; HoMA-IR, homeostasis model assessment of insulin resistance; FAI, free androgen index; L/A, leptin-to-adiponectin ratio. Fasting 25(OH)D, insulin, PED/PEA-15 protein abundance, leptin, and adiponectin values were not normally distributed and have been logarithmically transformed. PED/PEA-15 protein bands were quantified by laser densitometry and expressed as arbitrary units [13]. Bivariate correlations between variables were examined using Pearson's correlation coefficient and their values are singularly evidenced.
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Figure 1: Correlations between variables in the study population. 25(OH)D, 25(OH) Vitamin D; BMI, body mass index; HoMA-IR, homeostasis model assessment of insulin resistance; FAI, free androgen index; L/A, leptin-to-adiponectin ratio. Fasting 25(OH)D, insulin, PED/PEA-15 protein abundance, leptin, and adiponectin values were not normally distributed and have been logarithmically transformed. PED/PEA-15 protein bands were quantified by laser densitometry and expressed as arbitrary units [13]. Bivariate correlations between variables were examined using Pearson's correlation coefficient and their values are singularly evidenced.

Mentions: Correlations between variables in the study population were reported in Figure 1. In PCOS women, an inverse correlation was observed between 25(OH)D and BMI (a), PED/PEA-15 protein abundance (b), insulin (c), HoMA-IR (d), and FAI (e) (r= -0.474, -0.553, -0.380, -0.407, -0.374, respectively; p < 0.001), and L/A (f) (r= -0.306, p < 0.05). At the multivariate analysis, with PED/PEA-15 protein abundance as dependent variable only insulin and 25(OH)D remained in the model (β = 0.39 and β = -0.32, respectively) (Table 2). The results of the analysis were different, however, in the two group of PCOS women, as the major determinants of PED/PEA-15 protein abundance were BMI and insulin in lean PCOS (β = 0.65 and β = 0.26, respectively) (Table 3), and L/A, insulin and 25(OH)D in o/o PCOS (β = 0.45, β = 0.41 and β = -0.25, respectively) (Table 4).


Serum 25-Hydroxyvitamin D Levels, phosphoprotein enriched in diabetes gene product (PED/PEA-15) and leptin-to-adiponectin ratio in women with PCOS.

Savastano S, Valentino R, Di Somma C, Orio F, Pivonello C, Passaretti F, Brancato V, Formisano P, Colao A, Beguinot F, Tarantino G - Nutr Metab (Lond) (2011)

Correlations between variables in the study population. 25(OH)D, 25(OH) Vitamin D; BMI, body mass index; HoMA-IR, homeostasis model assessment of insulin resistance; FAI, free androgen index; L/A, leptin-to-adiponectin ratio. Fasting 25(OH)D, insulin, PED/PEA-15 protein abundance, leptin, and adiponectin values were not normally distributed and have been logarithmically transformed. PED/PEA-15 protein bands were quantified by laser densitometry and expressed as arbitrary units [13]. Bivariate correlations between variables were examined using Pearson's correlation coefficient and their values are singularly evidenced.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3293764&req=5

Figure 1: Correlations between variables in the study population. 25(OH)D, 25(OH) Vitamin D; BMI, body mass index; HoMA-IR, homeostasis model assessment of insulin resistance; FAI, free androgen index; L/A, leptin-to-adiponectin ratio. Fasting 25(OH)D, insulin, PED/PEA-15 protein abundance, leptin, and adiponectin values were not normally distributed and have been logarithmically transformed. PED/PEA-15 protein bands were quantified by laser densitometry and expressed as arbitrary units [13]. Bivariate correlations between variables were examined using Pearson's correlation coefficient and their values are singularly evidenced.
Mentions: Correlations between variables in the study population were reported in Figure 1. In PCOS women, an inverse correlation was observed between 25(OH)D and BMI (a), PED/PEA-15 protein abundance (b), insulin (c), HoMA-IR (d), and FAI (e) (r= -0.474, -0.553, -0.380, -0.407, -0.374, respectively; p < 0.001), and L/A (f) (r= -0.306, p < 0.05). At the multivariate analysis, with PED/PEA-15 protein abundance as dependent variable only insulin and 25(OH)D remained in the model (β = 0.39 and β = -0.32, respectively) (Table 2). The results of the analysis were different, however, in the two group of PCOS women, as the major determinants of PED/PEA-15 protein abundance were BMI and insulin in lean PCOS (β = 0.65 and β = 0.26, respectively) (Table 3), and L/A, insulin and 25(OH)D in o/o PCOS (β = 0.45, β = 0.41 and β = -0.25, respectively) (Table 4).

Bottom Line: Vitamin D is endowed with pleiotropic effects, including insulin resistance (IR) and apoptotic pathway.An inverse correlation was observed between 25(OH)D and BMI, PED/PEA-15 protein abundance, insulin, HoMA-IR, FAI (p < 0.001), and L/A (p < 0.05).Lower 25(OH)D and higher L/A were associated to PED/PEA-15 protein abundance in PCOS, suggesting their involvement in the ovarian imbalance between pro-and anti-apoptotic mechanisms, with high L/A and insulin and low 25(OH)D levels as the main determinants of PED/PEA-15 protein variability.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Molecular and Clinical Endocrinology and Oncology, Division of Endocrinology, University Federico II of Naples, Via S, Pansini 5, Naples, 80131, Italy. sisavast@unina.it.

ABSTRACT

Background: Polycystic ovary syndrome (PCOS) is frequently associated with hypovitaminosis D. Vitamin D is endowed with pleiotropic effects, including insulin resistance (IR) and apoptotic pathway. Disruption of the complex mechanism that regulated ovarian apoptosis has been reported in PCOS. Phosphoprotein enriched in diabetes gene product (PED/PEA-15), an anti-apoptotic protein involved in type 2 diabetes mellitus (T2DM), is overexpressed in PCOS women, independently of obesity. Leptin-to-adiponectin ratio (L/A) is a biomarker of IR and low-grade inflammation in PCOS. The aim of the study was to investigate the levels of 25-hydroxy vitamin D (25(OH)D), and L/A, in association with PED/PEA-15 protein abundance, in both lean and overweight/obese (o/o) women with PCOS.

Patients and methods: PED/PEA-15 protein abundance and circulating levels of 25(OH)D, L/A, sex hormone-binding globulin, and testosterone were evaluated in 90 untreated PCOS patients (25 ± 4 yrs; range 18-34) and 40 healthy controls age and BMI comparable, from the same geographical area. FAI (free androgen index) and the homeostasis model assessment of insulin resistance (HoMA-IR) index were calculated.

Results: In o/o PCOS, 25(OH)D levels were significantly lower, and L/A values were significantly higher than in lean PCOS (p < 0.001), while there were no differences in PED/PEA-15 protein abundance. An inverse correlation was observed between 25(OH)D and BMI, PED/PEA-15 protein abundance, insulin, HoMA-IR, FAI (p < 0.001), and L/A (p < 0.05). At the multivariate analysis, in o/o PCOS L/A, insulin and 25(OH)D were the major determinant of PED/PEA-15 protein abundance (β = 0.45, β = 0.41, and β = -0.25, respectively).

Conclusions: Lower 25(OH)D and higher L/A were associated to PED/PEA-15 protein abundance in PCOS, suggesting their involvement in the ovarian imbalance between pro-and anti-apoptotic mechanisms, with high L/A and insulin and low 25(OH)D levels as the main determinants of PED/PEA-15 protein variability. Further studies, involving also different apoptotic pathways or inflammatory cytokines and granulosa cells are mandatory to better define the possible bidirectional relationships between 25(OH)D, PED/PEA-15 protein abundance, leptin and adiponectin in PCOS pathogenesis.

No MeSH data available.


Related in: MedlinePlus