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Maternal vitamin D deficiency progra...

Nicholas, Cari Tishon.

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Maternal vitamin D deficiency programs reproductive dysfunction in adult female mice offspring.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Maternal vitamin D deficiency programs reproductive dysfunction in adult female mice offspring./
Author:	Nicholas, Cari Tishon.
Description:	169 p.
Notes:	Source: Dissertation Abstracts International, Volume: 77-09(E), Section: B.
Contained By:	Dissertation Abstracts International77-09B(E).
Subject:	Developmental biology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10117501
ISBN:	9781339788760

Maternal vitamin D deficiency programs reproductive dysfunction in adult female mice offspring.
Nicholas, Cari Tishon.

Maternal vitamin D deficiency programs reproductive dysfunction in adult female mice offspring. - 169 p.

Source: Dissertation Abstracts International, Volume: 77-09(E), Section: B.

Thesis (Ph.D.)--Yeshiva University, 2016.

Vitamin D is a fat soluble secosteroid produced in the endogenously skin, and is exogenously acquired from the diet. Vitamin D deficiency has reached near pandemic levels affecting over one billion people worldwide. This deficiency is most prevalent in the elderly, neonates, reproductive aged and pregnant women. The expression of VDR in the reproductive axis suggests that vitamin D signaling may be important for the development and function of the reproductive axis. The effect of exposure to maternal vitamin D on the reproductive physiology of the offspring has not been studied. We hypothesize that exposure to maternal vitamin D deficiency has adverse effects on the reproductive physiology of the female offspring during adulthood. Chapter 2 demonstrates that female offspring exposed to maternal vitamin D deficiency exhibited programmed estrous cycle dysfunction, which was characterized by extended periods of diestrus, attenuated preovulatory luteinizing hormone surges and oligoovulation in adulthood. In chapter 3, we validated that exposure to maternal vitamin D deficiency programmed reproductive abnormalities through primary hypothalamic dysfunction, in part by, misexpression of hypothalamic genes important for reproductive axis function. We propose that the misexpression of these genes may be caused of neuroendocrine vitamin D resistance in maternal vitamin D deficient females due to the overexpression of the heterogeneous nuclear ribonucleoproteins A (HnRNPAs) that inhibit VDR transactivation. Chapter 4 showed that maternal vitamin D deficiency caused misexpression of hypothalamic genes and gene ontology profiles showed changes in synaptic plasticity, neuron proliferation and development. In summary, vitamin D signaling is essential during early development for normal reproductive axis function in adulthood. Reproductive dysfunction in maternal vitamin D deficient female offspring may result from vitamin D resistance due to increased hypothalamic HnRNPAs, which inhibit VDR regulated expression of genes vital for reproductive function. The findings in this thesis provide novel insight in the field of reproductive endocrinology on how maternal nutritional vitamin D deficiency can have chronic effects on the development and function of the reproductive axis in exposed adult female offspring through fetal programming during early development.

ISBN: 9781339788760Subjects--Topical Terms:

592588
Developmental biology.

Maternal vitamin D deficiency programs reproductive dysfunction in adult female mice offspring.
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245 1 0 $a Maternal vitamin D deficiency programs reproductive dysfunction in adult female mice offspring.
300 $a 169 p.
500 $a Source: Dissertation Abstracts International, Volume: 77-09(E), Section: B.
500 $a Advisers: Genevieve Neal-Perry; Streamson Chua.
502 $a Thesis (Ph.D.)--Yeshiva University, 2016.
520 $a Vitamin D is a fat soluble secosteroid produced in the endogenously skin, and is exogenously acquired from the diet. Vitamin D deficiency has reached near pandemic levels affecting over one billion people worldwide. This deficiency is most prevalent in the elderly, neonates, reproductive aged and pregnant women. The expression of VDR in the reproductive axis suggests that vitamin D signaling may be important for the development and function of the reproductive axis. The effect of exposure to maternal vitamin D on the reproductive physiology of the offspring has not been studied. We hypothesize that exposure to maternal vitamin D deficiency has adverse effects on the reproductive physiology of the female offspring during adulthood. Chapter 2 demonstrates that female offspring exposed to maternal vitamin D deficiency exhibited programmed estrous cycle dysfunction, which was characterized by extended periods of diestrus, attenuated preovulatory luteinizing hormone surges and oligoovulation in adulthood. In chapter 3, we validated that exposure to maternal vitamin D deficiency programmed reproductive abnormalities through primary hypothalamic dysfunction, in part by, misexpression of hypothalamic genes important for reproductive axis function. We propose that the misexpression of these genes may be caused of neuroendocrine vitamin D resistance in maternal vitamin D deficient females due to the overexpression of the heterogeneous nuclear ribonucleoproteins A (HnRNPAs) that inhibit VDR transactivation. Chapter 4 showed that maternal vitamin D deficiency caused misexpression of hypothalamic genes and gene ontology profiles showed changes in synaptic plasticity, neuron proliferation and development. In summary, vitamin D signaling is essential during early development for normal reproductive axis function in adulthood. Reproductive dysfunction in maternal vitamin D deficient female offspring may result from vitamin D resistance due to increased hypothalamic HnRNPAs, which inhibit VDR regulated expression of genes vital for reproductive function. The findings in this thesis provide novel insight in the field of reproductive endocrinology on how maternal nutritional vitamin D deficiency can have chronic effects on the development and function of the reproductive axis in exposed adult female offspring through fetal programming during early development.
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