Bibliography: leaves 105-151. / xi, 151, [47] leaves, [3] leaves of plates : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This thesis examines the effect of remodelling HDL on the metabolism of apo A-I. The major focus is on the effects of CETP and LCAT in the regulation of apo A-I concentration in DHL. The effects of incubation of HDL with CETP in the presence of VLDL and/or LDL on apo A-I concentration in HDL are examined. The characterization of the dissociated apo A-I from HDL is presented. The studies demonstrate that the dissociation of apo A-I from HDL mediated by CETP is preventable and reversible in a process dependent on LCAT activity. The mechanism by which HDL apo A-I content is increased is also explored. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1997?

Bibliography: leaves 105-151. / xi, 151, [47] leaves, [3] leaves of plates : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This thesis examines the effect of remodelling HDL on the metabolism of apo A-I. The major focus is on the effects of CETP and LCAT in the regulation of apo A-I concentration in DHL. The effects of incubation of HDL with CETP in the presence of VLDL and/or LDL on apo A-I concentration in HDL are examined. The characterization of the dissociated apo A-I from HDL is presented. The studies demonstrate that the dissociation of apo A-I from HDL mediated by CETP is preventable and reversible in a process dependent on LCAT activity. The mechanism by which HDL apo A-I content is increased is also explored. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1997?

Thesis (Ph.D.)--Tufts University, 2004. / Adviser: Alice H. Lichtenstein. Submitted to the School of Nutrition Science and Policy. Includes bibliographical references. Access restricted to members of the Tufts University community. Also available via the World Wide Web;

This study was designed to investigate the mechanism(s) underlying the hypercatabolism of high density lipoprotein in Tangier disease (TD). Initially, the metabolism of normal HDL incubated in Tangier plasma in vitro was examined. Sufficient normal human HDL was added to TD plasma to raise the concentration of HDL-cholesterol to within normal levels. During incubation the concentration of HDL-cholesterol in the TD plasma fell by up to 50% in a time dependent manner. This was not seen in control samples treated in a similar manner. The loss of HDL-cholesterol in the TD could be completely accounted for by the loss of HDL-cholesteryl ester and was accompanied by a 2.3-fold increase in the concentration of HDL-triglyceride. These observations could not be accounted for by lecithin: cholesterol acytransferase activity, cholesteryl ester hydrolysis, or the triglyceride level in the TD plasma. However, preliminary evidence suggested that the activity of cholesteryl ester transfer protein in TD plasma is responsible for the changes in HDL-lipid composition. The resulting triglyceride-rich, cholesteryl-poor HDL was shown to have a normal affinity for the human skin fibroblast HDL receptor. However, this finding does not exclude other pathways of HDL catabolism that may contribute to the rapid turnover of modified HDL in TD plasma. The metabolism of normal HDL by TD fibroblasts and monocytes in vitro was also studied in an attempt to identify a cellular defect of HDL metabolism in TD. However, both TD fibroblasts and monocytes were normal with respect to their ability to bind/internalize and degrade normal HDL invitro. It is concluded that the hypercatabolism of normal HDL in TD involves alterations of HDL-lipid and protein composition prior to removal from the plasma component. Thus, these studies support the hypothesis that the defect in TD resides in the plasma and not in the cells of these patients. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

Insulin resistance and type 2 diabetes are pathogenetically linked to increased risk of cardiovascular disease. While insulin resistance is defined by a dysregulation in hepatic insulin signaling, it is unclear how this impairment relates to the development of cardiovascular disease. Recently, there has been evidence showing that in insulin resistant individuals, cardiovascular disease is associated with a defect in reverse cholesterol transport – the cardioprotective process by which excess cholesterol is removed from the periphery, and returned to the liver for biliary excretion. Reverse cholesterol transport is facilitated by high-density lipoprotein (HDL) metabolism. Thus, malfunction in HDL turnover during reverse cholesterol transport may contribute to the buildup of atherosclerotic plaques, and subsequent cardiovascular disease in insulin resistant individuals. In this thesis, we seek to establish a better understanding of HDL metabolism and reverse cholesterol transport, as they relate to key transcription factors that mediate hepatic insulin signaling, namely the insulin-repressible forkhead transcription factors, FoxO1, FoxO3, and FoxO4 (FoxOs). We demonstrate that mice with liver-specific triple FoxO knockout (L-FoxO1,3,4) have increased HDL-cholesterol (HDL-C), associated with decreased expression of HDL-C clearance factors, scavenger receptor class B type I (SR-BI) and hepatic lipase, and defective selective uptake of HDL-cholesteryl ester by the liver. As such, we uncover a novel mechanism by which HDL-mediated reverse cholesterol transport to the liver is regulated by the hepatic insulin-->FoxO signaling pathway.

Thesis (Ph. D.)--University of Washington, 2004. / Vita. Includes bibliographical references (leaves 138-149).

Thesis (Ph.D.)--University of Western Australia, 2007.

Thesis (Ph. D.)--University of Missouri-Columbia, 1997. / Typescript. Vita. Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 1997. / Typescript. Vita. Includes bibliographical references. Also available on the Internet.

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