Effects of Vitamin D Deficiency on Proliferation and Autophagy of Ovarian and Liver Tissues in a Rat Model of Polycystic Ovary Syndrome

Krisztina Lajtai, Csilla Terézia Nagy, Róbert Tarszabó, Rita Benkő, Leila Hadjadj, Réka Eszter Sziva, Dóra Gerszi, Bálint Bányai, Péter Ferdinandy, G. Nádasy, Z. Giricz, Eszter Mária Horváth, S. Várbíró

Research output: Article

Abstract

AIM: We aimed to examine the alterations of the insulin signaling pathway, autophagy, nitrative stress and the effect of vitamin D supplementation in the liver and ovaries of vitamin D deficient hyperandrogenic rats. METHODS: Female Wistar rats received eight weeks of transdermal testosterone treatment and lived on a low vitamin D diet (D-T+). Vitamin D supplementation was achieved by oral administration of vitamin D3 (D+T+). Sham-treated (D+T-) and vitamin D deficient animals (D-T-) served as controls. (N = 10-12 per group). RESULTS: D-T+ animals showed decreased LC3 II levels in the liver and increased p-Akt/Akt and p-eNOS/eNOS ratios with decreased insulin receptor staining in the ovaries. Vitamin D supplementation prevented the increase of Akt phosphorylation in the ovaries. Vitamin D deficiency itself also led to decreased LC3 II levels in the liver and decreased insulin receptor staining in the ovaries. D-T+ group showed no increase in nitrotyrosine staining; however, the ovaries of D-T- rats and the liver of D+T+ animals showed increased staining intensity. CONCLUSION: Vitamin D deficiency itself might lead to disrupted ovarian maturation and autophagy malfunction in the liver. Preventing Akt phosphorylation may contribute to the beneficial effect of vitamin D treatment on ovarian function in hyperandrogenism.

Original languageEnglish
JournalBiomolecules
Volume9
Issue number9
DOIs
Publication statusPublished - szept. 10 2019

Fingerprint

Vitamin D Deficiency
Polycystic Ovary Syndrome
Autophagy
Vitamin D
Liver
Rats
Tissue
Ovary
Staining and Labeling
Insulin Receptor
Phosphorylation
Animals
Hyperandrogenism
Cholecalciferol
Nutrition
Oral Administration
Testosterone
Wistar Rats
Insulin
Diet

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

Cite this

Effects of Vitamin D Deficiency on Proliferation and Autophagy of Ovarian and Liver Tissues in a Rat Model of Polycystic Ovary Syndrome. / Lajtai, Krisztina; Nagy, Csilla Terézia; Tarszabó, Róbert; Benkő, Rita; Hadjadj, Leila; Sziva, Réka Eszter; Gerszi, Dóra; Bányai, Bálint; Ferdinandy, Péter; Nádasy, G.; Giricz, Z.; Horváth, Eszter Mária; Várbíró, S.

In: Biomolecules, Vol. 9, No. 9, 10.09.2019.

Research output: Article

Lajtai, Krisztina ; Nagy, Csilla Terézia ; Tarszabó, Róbert ; Benkő, Rita ; Hadjadj, Leila ; Sziva, Réka Eszter ; Gerszi, Dóra ; Bányai, Bálint ; Ferdinandy, Péter ; Nádasy, G. ; Giricz, Z. ; Horváth, Eszter Mária ; Várbíró, S. / Effects of Vitamin D Deficiency on Proliferation and Autophagy of Ovarian and Liver Tissues in a Rat Model of Polycystic Ovary Syndrome. In: Biomolecules. 2019 ; Vol. 9, No. 9.
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abstract = "AIM: We aimed to examine the alterations of the insulin signaling pathway, autophagy, nitrative stress and the effect of vitamin D supplementation in the liver and ovaries of vitamin D deficient hyperandrogenic rats. METHODS: Female Wistar rats received eight weeks of transdermal testosterone treatment and lived on a low vitamin D diet (D-T+). Vitamin D supplementation was achieved by oral administration of vitamin D3 (D+T+). Sham-treated (D+T-) and vitamin D deficient animals (D-T-) served as controls. (N = 10-12 per group). RESULTS: D-T+ animals showed decreased LC3 II levels in the liver and increased p-Akt/Akt and p-eNOS/eNOS ratios with decreased insulin receptor staining in the ovaries. Vitamin D supplementation prevented the increase of Akt phosphorylation in the ovaries. Vitamin D deficiency itself also led to decreased LC3 II levels in the liver and decreased insulin receptor staining in the ovaries. D-T+ group showed no increase in nitrotyrosine staining; however, the ovaries of D-T- rats and the liver of D+T+ animals showed increased staining intensity. CONCLUSION: Vitamin D deficiency itself might lead to disrupted ovarian maturation and autophagy malfunction in the liver. Preventing Akt phosphorylation may contribute to the beneficial effect of vitamin D treatment on ovarian function in hyperandrogenism.",
keywords = "autophagy, hyperandrogenism, insulin resistance, oxidative stress, polycystic ovary syndrome (PCOS), vitamin D",
author = "Krisztina Lajtai and Nagy, {Csilla Ter{\'e}zia} and R{\'o}bert Tarszab{\'o} and Rita Benkő and Leila Hadjadj and Sziva, {R{\'e}ka Eszter} and D{\'o}ra Gerszi and B{\'a}lint B{\'a}nyai and P{\'e}ter Ferdinandy and G. N{\'a}dasy and Z. Giricz and Horv{\'a}th, {Eszter M{\'a}ria} and S. V{\'a}rb{\'i}r{\'o}",
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T1 - Effects of Vitamin D Deficiency on Proliferation and Autophagy of Ovarian and Liver Tissues in a Rat Model of Polycystic Ovary Syndrome

AU - Lajtai, Krisztina

AU - Nagy, Csilla Terézia

AU - Tarszabó, Róbert

AU - Benkő, Rita

AU - Hadjadj, Leila

AU - Sziva, Réka Eszter

AU - Gerszi, Dóra

AU - Bányai, Bálint

AU - Ferdinandy, Péter

AU - Nádasy, G.

AU - Giricz, Z.

AU - Horváth, Eszter Mária

AU - Várbíró, S.

PY - 2019/9/10

Y1 - 2019/9/10

N2 - AIM: We aimed to examine the alterations of the insulin signaling pathway, autophagy, nitrative stress and the effect of vitamin D supplementation in the liver and ovaries of vitamin D deficient hyperandrogenic rats. METHODS: Female Wistar rats received eight weeks of transdermal testosterone treatment and lived on a low vitamin D diet (D-T+). Vitamin D supplementation was achieved by oral administration of vitamin D3 (D+T+). Sham-treated (D+T-) and vitamin D deficient animals (D-T-) served as controls. (N = 10-12 per group). RESULTS: D-T+ animals showed decreased LC3 II levels in the liver and increased p-Akt/Akt and p-eNOS/eNOS ratios with decreased insulin receptor staining in the ovaries. Vitamin D supplementation prevented the increase of Akt phosphorylation in the ovaries. Vitamin D deficiency itself also led to decreased LC3 II levels in the liver and decreased insulin receptor staining in the ovaries. D-T+ group showed no increase in nitrotyrosine staining; however, the ovaries of D-T- rats and the liver of D+T+ animals showed increased staining intensity. CONCLUSION: Vitamin D deficiency itself might lead to disrupted ovarian maturation and autophagy malfunction in the liver. Preventing Akt phosphorylation may contribute to the beneficial effect of vitamin D treatment on ovarian function in hyperandrogenism.

AB - AIM: We aimed to examine the alterations of the insulin signaling pathway, autophagy, nitrative stress and the effect of vitamin D supplementation in the liver and ovaries of vitamin D deficient hyperandrogenic rats. METHODS: Female Wistar rats received eight weeks of transdermal testosterone treatment and lived on a low vitamin D diet (D-T+). Vitamin D supplementation was achieved by oral administration of vitamin D3 (D+T+). Sham-treated (D+T-) and vitamin D deficient animals (D-T-) served as controls. (N = 10-12 per group). RESULTS: D-T+ animals showed decreased LC3 II levels in the liver and increased p-Akt/Akt and p-eNOS/eNOS ratios with decreased insulin receptor staining in the ovaries. Vitamin D supplementation prevented the increase of Akt phosphorylation in the ovaries. Vitamin D deficiency itself also led to decreased LC3 II levels in the liver and decreased insulin receptor staining in the ovaries. D-T+ group showed no increase in nitrotyrosine staining; however, the ovaries of D-T- rats and the liver of D+T+ animals showed increased staining intensity. CONCLUSION: Vitamin D deficiency itself might lead to disrupted ovarian maturation and autophagy malfunction in the liver. Preventing Akt phosphorylation may contribute to the beneficial effect of vitamin D treatment on ovarian function in hyperandrogenism.

KW - autophagy

KW - hyperandrogenism

KW - insulin resistance

KW - oxidative stress

KW - polycystic ovary syndrome (PCOS)

KW - vitamin D

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U2 - 10.3390/biom9090471

DO - 10.3390/biom9090471

M3 - Article

C2 - 31509973

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VL - 9

JO - Biomolecules

JF - Biomolecules

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