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You searched for subject:(fetal cholesterol metabolism). Showing records 1 – 2 of 2 total matches.

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University of Cincinnati

1. SCHMID, KARA E. ENDOGENOUS AND EXOGENOUS SOURCES OF CHOLESTEROL DURING FETAL DEVELOPMENT.

Degree: PhD, Medicine : Pathobiology and Molecular Medicine, 2003, University of Cincinnati

Cholesterol is essential for proper fetal development. Defects in fetal cholesterol metabolism can cause developmental abnormalities, including mental retardation and stunted growth as demonstrated by patients with Smith-Lemli-Optiz syndrome. Understanding fetal cholesterol metabolism could lead to the development of a method to prevent or lessen cholesterol deficiency related birth defects. Therefore, the goal of this dissertation was to examine cholesterol metabolism in the developing fetus. Understanding cholesterol metabolism requires the examination of both sources of cholesterol: cholesterol synthesized de novo and cholesterol provided exogenously. De novo cholesterol synthesis in the adult can be regulated by dietary polyunsaturated fatty acids. If fetal cholesterol synthesis rates are regulated as in the adult, then the consumption of polyunsaturated fatty acids during pregnancy may have an impact on fetal development. Therefore, the regulation of cholesterol synthesis in the fetus was examined. Pregnant hamsters were fed various fatty acids throughout gestation and sterol synthesis rates in the fetus were determined. Although the rate of sterol synthesis in the adult hamster was decreased by dietary polyunsaturated fatty acids, sterol synthesis rates in the fetus were unaffected. In addition, the adult could be made to become unresponsive to dietary polyunsaturated fatty acids by inducing a negative sterol balance across the liver. These data demonstrated that sterol synthesis is regulated differently in fetal tissues as compared to adults, possibly due to a negative sterol balance in the fetus. The placenta regulates the transport of exogenous nutrients from the maternal circulation to the fetal circulation. The placental transport of glucose and fatty acids is well established, however the transport of cholesterol remains undefined. Therefore, a human choriocarcinoma cell line, BeWo, was utilized to model the transport of cholesterol across a placental monolayer. It was demonstrated that cholesterol could be transported from the apical surface of the placental cell to the basolateral surface for efflux to components of fetal human serum, fetal HDL and phospholipid vesicles but not apolipoprotein A-I. BeWo cells demonstrated a mass movement of cholesterol from the apical to basolateral chamber that could be manipulated by increasing the cellular cholesterol concentration. These were the first studies to utilize an in vitro model to demonstrate the transport of cholesterol from the maternal circulation (apical side) to the fetal circulation (basolateral side). Understanding and dissecting this pathway may aid in the development of in utero treatments for fetuses with defects in cholesterol biosynthesis. Advisors/Committee Members: Woollett, Dr. Laura A. (Advisor).

Subjects/Keywords: Biophysics, Medical; fetal cholesterol metabolism; placental transport; cholesterol synthesis; Smith-Lemli-Optiz

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

SCHMID, K. E. (2003). ENDOGENOUS AND EXOGENOUS SOURCES OF CHOLESTEROL DURING FETAL DEVELOPMENT. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1061304521

Chicago Manual of Style (16th Edition):

SCHMID, KARA E. “ENDOGENOUS AND EXOGENOUS SOURCES OF CHOLESTEROL DURING FETAL DEVELOPMENT.” 2003. Doctoral Dissertation, University of Cincinnati. Accessed April 12, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1061304521.

MLA Handbook (7th Edition):

SCHMID, KARA E. “ENDOGENOUS AND EXOGENOUS SOURCES OF CHOLESTEROL DURING FETAL DEVELOPMENT.” 2003. Web. 12 Apr 2021.

Vancouver:

SCHMID KE. ENDOGENOUS AND EXOGENOUS SOURCES OF CHOLESTEROL DURING FETAL DEVELOPMENT. [Internet] [Doctoral dissertation]. University of Cincinnati; 2003. [cited 2021 Apr 12]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1061304521.

Council of Science Editors:

SCHMID KE. ENDOGENOUS AND EXOGENOUS SOURCES OF CHOLESTEROL DURING FETAL DEVELOPMENT. [Doctoral Dissertation]. University of Cincinnati; 2003. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1061304521

2. Sohi, Gurjeev. Molecular Mechanisms Underlying the Early Life Programming of the Liver.

Degree: 2013, University of Western Ontario

Clinical studies have demonstrated that intrauterine growth restriction (IUGR) offspring, faced with a nutritional mismatch postpartum, have an increased risk of developing the metabolic syndrome. The maternal protein restriction (MPR) rat model has been extensively studied to investigate the adverse effects of a nutritional mismatch in postnatal life of IUGR offspring. Previous studies have demonstrated that MPR leads to impaired function of the liver, an important metabolic organ. However the underlying mechanisms which predispose these offspring to the metabolic syndrome remain elusive. In the following studies, low protein diet during pregnancy and lactation led to IUGR offspring with decreased liver to body weight ratios, followed by increased circulating and hepatic cholesterol levels in both sexes at day 21 and exclusively in the male offspring at day 130. This was attributed to long-term repressive changes in histone modifications at the promoter of cholesterol 7α-hydroxylase, a rate-limiting enzyme that catabolizes cholesterol to bile acids. It was later demonstrated that these IUGR offspring exhibited increased molecular markers of hepatic endoplasmic reticulum (ER) stress and insulin resistance. Finally, these offspring were observed to have an increase in activity of Phase I drug metabolizing hepatic cytochrome p450 (Cyp) dependent enzymes. Collectively, these findings suggest that stable promoter-specific changes to post-translational histone modifications and elevated ER stress in the liver, are key molecular mechanisms whereby IUGR offspring receiving a nutritional mismatch in postnatal life develop high cholesterol and insulin resistance. Moreover, these offspring may require augmented doses of drugs in order to alleviate these symptoms.

Subjects/Keywords: Fetal Programming; Intrauterine Growth Restriction; Thrifty Phenotype; Low Protein Diet; Metabolic Syndrome; Cholesterol; Insulin Resistance; Liver; Epigenetics; Posttranslational Histone Modifications; Endoplasmic Reticulum Stress; Protein Translation; Growth; Drug Metabolism; Developmental Biology; Endocrinology; Life Sciences; Molecular Biology; Nutrition; Pharmacology; Physiology

…correlation of fetal growth to elevated cholesterol levels and glucose intolerance in adult life was… …programming of adult cholesterol metabolism, type 2 diabetes and ischemic heart disease. First and… …weight and plasma cholesterol levels, but an increase in fetal hepatic cholesterol77. In… …and uptake, and cholesterol metabolism and efflux113, 114. The LXR/RXR heterodimer can be… …Tolerance 9 viii 1.6.1 Effects of Hypoxia on Long-term Cholesterol and Glucose Homeostasis 9… 

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Sohi, G. (2013). Molecular Mechanisms Underlying the Early Life Programming of the Liver. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/1455

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Sohi, Gurjeev. “Molecular Mechanisms Underlying the Early Life Programming of the Liver.” 2013. Thesis, University of Western Ontario. Accessed April 12, 2021. https://ir.lib.uwo.ca/etd/1455.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Sohi, Gurjeev. “Molecular Mechanisms Underlying the Early Life Programming of the Liver.” 2013. Web. 12 Apr 2021.

Vancouver:

Sohi G. Molecular Mechanisms Underlying the Early Life Programming of the Liver. [Internet] [Thesis]. University of Western Ontario; 2013. [cited 2021 Apr 12]. Available from: https://ir.lib.uwo.ca/etd/1455.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sohi G. Molecular Mechanisms Underlying the Early Life Programming of the Liver. [Thesis]. University of Western Ontario; 2013. Available from: https://ir.lib.uwo.ca/etd/1455

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

.