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Maternal Hypercholesterolemia Progra...

Dumolt, Jerad H.

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Maternal Hypercholesterolemia Programs Nonalcoholic Fatty Liver Disease in Offspring of ApoE Deficient Mice.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Maternal Hypercholesterolemia Programs Nonalcoholic Fatty Liver Disease in Offspring of ApoE Deficient Mice./
作者:	Dumolt, Jerad H.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
面頁冊數:	115 p.
附註:	Source: Dissertations Abstracts International, Volume: 81-05, Section: B.
Contained By:	Dissertations Abstracts International81-05B.
標題:	Nutrition. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=22587376
ISBN:	9781088366448

Maternal Hypercholesterolemia Programs Nonalcoholic Fatty Liver Disease in Offspring of ApoE Deficient Mice.
Dumolt, Jerad H.

Maternal Hypercholesterolemia Programs Nonalcoholic Fatty Liver Disease in Offspring of ApoE Deficient Mice. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 115 p.

Source: Dissertations Abstracts International, Volume: 81-05, Section: B.

Thesis (Ph.D.)--State University of New York at Buffalo, 2019.

This item must not be sold to any third party vendors.

Maternal hypercholesterolemia (MHC) is a pathological condition characterized by an exaggerated rise in maternal serum cholesterol during pregnancy which can program metabolic dysfunction in offspring including dysregulation of hepatic lipid metabolism. There are several unanswered questions regarding this condition particularly with regard to how the timing of cholesterol exposure influences hepatic lipid dysfunction and the mechanisms through which these adaptations manifest in adulthood. The purpose of this dissertation was to: (i) assess the influence of the postnatal diet in programming nonalcoholic fatty liver disease (NAFLD) in adult offspring from MHC mothers; (ii) determine the degree to which in utero exposure to excess cholesterol affects fetal lipid status and the molecular mechanisms involved; and (iii) determine the extent to which exposure to gestational hypercholesterolemia differentially programs the development of NAFLD in newly-weaned and adult male and female progeny.MHC was induced in apolipoprotein-E deficient (apoE-/-) mice by feeding a standard chow diet (CON) or the CON diet enriched in cholesterol (CH, 0.15% wt:wt). MHC was induced both throughout gestation and lactation and in the gestation period only. Metabolic programming effects were examined in offspring fed postnatal control and western style diets and sex effects were examined. Adult offspring exposed to MHC throughout both gestation and lactation and fed a postnatal CON diet had an atherogenic lipid profile and increased hepatic cholesterol and triglyceride (TG) content with altered lipid regulatory mRNA expression and protein content. However, these changes were not apparent when a postnatal western style diet was fed, suggesting a potential masking effect of excess postnatal nutrient intake. Excessive cholesterol exposure in the gestation period only increased fetal hepatic TG and altered the mRNA and microRNA expression of lipid regulatory genes in the liver. Newly-weaned and adult male offspring exposed to MHC in the gestation period only had similar serum and hepatic lipid profiles compared to males exposed throughout gestation and lactation. Further, while programming effects were largely absent in female offspring, sex-divergent lipid responses to elevated maternal cholesterol was apparent between male and females from similar exposure windows.In summary, MHC altered fetal hepatic lipid metabolism and programmed NAFLD in adult offspring. Further, the degree of hepatic lipid dysfunction in adult offspring was similar whether MHC was induced in gestation or throughout both the gestation and lactation periods. Lastly, malprogramming of hepatic lipid metabolism largely occurs in a sex-specific manner with males appearing to be more susceptible compared with their female counterparts.

ISBN: 9781088366448Subjects--Topical Terms:

517777
Nutrition.
Subjects--Index Terms:

Maternal hypercholesterolemia

Maternal Hypercholesterolemia Programs Nonalcoholic Fatty Liver Disease in Offspring of ApoE Deficient Mice.
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520 $a Maternal hypercholesterolemia (MHC) is a pathological condition characterized by an exaggerated rise in maternal serum cholesterol during pregnancy which can program metabolic dysfunction in offspring including dysregulation of hepatic lipid metabolism. There are several unanswered questions regarding this condition particularly with regard to how the timing of cholesterol exposure influences hepatic lipid dysfunction and the mechanisms through which these adaptations manifest in adulthood. The purpose of this dissertation was to: (i) assess the influence of the postnatal diet in programming nonalcoholic fatty liver disease (NAFLD) in adult offspring from MHC mothers; (ii) determine the degree to which in utero exposure to excess cholesterol affects fetal lipid status and the molecular mechanisms involved; and (iii) determine the extent to which exposure to gestational hypercholesterolemia differentially programs the development of NAFLD in newly-weaned and adult male and female progeny.MHC was induced in apolipoprotein-E deficient (apoE-/-) mice by feeding a standard chow diet (CON) or the CON diet enriched in cholesterol (CH, 0.15% wt:wt). MHC was induced both throughout gestation and lactation and in the gestation period only. Metabolic programming effects were examined in offspring fed postnatal control and western style diets and sex effects were examined. Adult offspring exposed to MHC throughout both gestation and lactation and fed a postnatal CON diet had an atherogenic lipid profile and increased hepatic cholesterol and triglyceride (TG) content with altered lipid regulatory mRNA expression and protein content. However, these changes were not apparent when a postnatal western style diet was fed, suggesting a potential masking effect of excess postnatal nutrient intake. Excessive cholesterol exposure in the gestation period only increased fetal hepatic TG and altered the mRNA and microRNA expression of lipid regulatory genes in the liver. Newly-weaned and adult male offspring exposed to MHC in the gestation period only had similar serum and hepatic lipid profiles compared to males exposed throughout gestation and lactation. Further, while programming effects were largely absent in female offspring, sex-divergent lipid responses to elevated maternal cholesterol was apparent between male and females from similar exposure windows.In summary, MHC altered fetal hepatic lipid metabolism and programmed NAFLD in adult offspring. Further, the degree of hepatic lipid dysfunction in adult offspring was similar whether MHC was induced in gestation or throughout both the gestation and lactation periods. Lastly, malprogramming of hepatic lipid metabolism largely occurs in a sex-specific manner with males appearing to be more susceptible compared with their female counterparts.
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