MARC Record from marc_columbia

LEADER: 02912cam a22003853i 4500
001 14840806
005 20200521220425.0
006 m o d
007 cr |n||||a||||
008 200428s2019 nyu|||| om 00| ||eng d
035 $a(OCoLC)1087188448
035 $a(OCoLC)on1087188448
035 $a(NNC)ACfeed:legacy_id:ac:nk98sf7m3k
035 $a(NNC)ACfeed:doi:10.7916/d8-yzmw-9347
035 $a(NNC)14840806
040 $aNNC$beng$erda$cNNC
100 1 $aLee, Samuel.
245 10 $aInsulin Regulation of Reverse Cholesterol Transport /$cSamuel Lee.
264 1 $a[New York, N.Y.?] :$b[publisher not identified],$c2019.
336 $atext$btxt$2rdacontent
337 $acomputer$bc$2rdamedia
338 $aonline resource$bcr$2rdacarrier
300 $a1 online resource.
502 $aThesis (Ph.D.)--Columbia University, 2019.
500 $aDepartment: Nutritional and Metabolic Biology.
500 $aThesis advisor: Rebecca A. Haeusler.
520 $aInsulin 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).
520 $aWe 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.
653 0 $aNutrition
653 0 $aBiology
653 0 $aHigh density lipoproteins--Metabolism
653 0 $aInsulin resistance
653 0 $aCholesterol
856 40 $uhttps://doi.org/10.7916/d8-yzmw-9347$zClick for full text
852 8 $blweb$hDISSERTATIONS