{"id":{"repo_id":"wfu","oai_identifier":"oai:wakespace.lib.wfu.edu:10339/30432"},"canonical_url":"https://search.dev.ndltd.org/etd/wfu/oai:wakespace.lib.wfu.edu:10339/30432","repository":{"repo_id":"wfu","name":"Wake Forest University","base_url":"https://wakespace.lib.wfu.edu/oai/request"},"display":{"title":"THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES","abstract":"Niemann-Pick C1-Like 1 (NPC1L1) is a polytopic transmembrane protein critical for intestinal absorption of dietary and biliary cholesterol. Ezetimibe, by inhibiting NPC1L1 function, is widely used to lower blood cholesterol in humans. Recently, NPC1L1 deficiency or ezetimibe treatment has been shown to improve hepatic steatosis in rodents and humans without a defined mechanism. In the first project, we found that genetic inactivation of NPC1L1 in mice prevents high fat diet (HFD)-induced fatty liver by inhibiting hepatic de novo lipogenesis, at least in part, through protecting mice against HFD-induced insulin resistance and hyperinsulinemia, a state known to drive hepatic lipogenesis. .","abstract_html":"Niemann-Pick C1-Like 1 (NPC1L1) is a polytopic transmembrane protein critical for intestinal absorption of dietary and biliary cholesterol. Ezetimibe, by inhibiting NPC1L1 function, is widely used to lower blood cholesterol in humans. Recently, NPC1L1 deficiency or ezetimibe treatment has been shown to improve hepatic steatosis in rodents and humans without a defined mechanism. In the first project, we found that genetic inactivation of NPC1L1 in mice prevents high fat diet (HFD)-induced fatty liver by inhibiting hepatic de novo lipogenesis, at least in part, through protecting mice against HFD-induced insulin resistance and hyperinsulinemia, a state known to drive hepatic lipogenesis. .","abstract_has_math":false,"creators":["Jia, Lin"],"institution":"Wake Forest University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010","date_published":"2010","updated_at":"2026-07-27T22:01:14Z","subjects":["Cholesterol"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10339/30432","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Jia, Lin"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2011-02-16T21:42:40Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2012-11-24T09:30:07Z"]},{"key":"dc:date.issued","label":"Date","values":["2010"]},{"key":"dc:publisher","label":"Institution","values":["Wake Forest University"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Cholesterol"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10339/30432"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Niemann-Pick C1-Like 1 (NPC1L1) is a polytopic transmembrane protein critical for intestinal absorption of dietary and biliary cholesterol. Ezetimibe, by inhibiting NPC1L1 function, is widely used to lower blood cholesterol in humans. Recently, NPC1L1 deficiency or ezetimibe treatment has been shown to improve hepatic steatosis in rodents and humans without a defined mechanism. In the first project, we found that genetic inactivation of NPC1L1 in mice prevents high fat diet (HFD)-induced fatty liver by inhibiting hepatic de novo lipogenesis, at least in part, through protecting mice against HFD-induced insulin resistance and hyperinsulinemia, a state known to drive hepatic lipogenesis. ."]},{"key":"dc:title","label":"Title","values":["THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES"]}]}],"canonical_facts":{"dc:creator":["Jia, Lin"],"dc:date.accessioned":["2011-02-16T21:42:40Z"],"dc:date.available":["2012-11-24T09:30:07Z"],"dc:date.issued":["2010"],"dc:description.abstract":["Niemann-Pick C1-Like 1 (NPC1L1) is a polytopic transmembrane protein critical for intestinal absorption of dietary and biliary cholesterol. Ezetimibe, by inhibiting NPC1L1 function, is widely used to lower blood cholesterol in humans. Recently, NPC1L1 deficiency or ezetimibe treatment has been shown to improve hepatic steatosis in rodents and humans without a defined mechanism. In the first project, we found that genetic inactivation of NPC1L1 in mice prevents high fat diet (HFD)-induced fatty liver by inhibiting hepatic de novo lipogenesis, at least in part, through protecting mice against HFD-induced insulin resistance and hyperinsulinemia, a state known to drive hepatic lipogenesis. ."],"dc:identifier.uri":["http://hdl.handle.net/10339/30432"],"dc:language.iso":["en"],"dc:publisher":["Wake Forest University"],"dc:subject":["Cholesterol"],"dc:title":["THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES"],"dc:type":["Dissertation"]},"updated_at":"2026-07-27T22:01:14Z"}