{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/129686"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/129686","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Novel regulation of hepatic lipid secretion and storage","abstract":"Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2027-05-01","abstract_html":"Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2027-05-01","abstract_has_math":false,"creators":["Lu, Wei"],"institution":"University of Illinois Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"VMS - Comparative Biosciences","degree_department":null,"school":null,"contributors":["Wang, Bo","Nelson, Erik","Spinella, Michael J","Yang, Jing"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2025,"date_issued":"2025-04-15","date_published":"2025-04-15","updated_at":"2026-07-22T22:25:05Z","subjects":["Atherosclerosis","VLDL","ApoB lipidation","lipid droplet expansion"],"languages":["en","eng"],"rights":["Copyright 2025 Wei Lu"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://hdl.handle.net/2142/129686","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Wang, Bo","Nelson, Erik","Spinella, Michael J","Yang, Jing"]},{"key":"dc:creator","label":"Author","values":["Lu, Wei"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2025-04-15","2025-05"]},{"key":"dc:type","label":"Dc Type","values":["text","Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["VMS - Comparative Biosciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Atherosclerosis","VLDL","ApoB lipidation","lipid droplet expansion"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en","eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 2025 Wei Lu"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://hdl.handle.net/2142/129686"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2027-05-01","The student, Wei Lu, accepted the attached license on 2025-04-14 at 11:41.","The student, Wei Lu, submitted this Dissertation for approval on 2025-04-14 at 11:54.","This Dissertation was approved for publication on 2025-04-15 at 16:42.","DSpace SAF Submission Ingestion Package generated from Vireo submission #21764 on 2025-10-19 at 19:52:50","The liver plays a critical role in lipid homeostasis, where lipids are either secreted as very-low-density lipoproteins (VLDL) or stored in lipid droplets. Previous studies have demonstrated a close relationship between VLDL and lipid droplet metabolism. Impaired VLDL secretion has been associated with increased lipid droplet formation, whereas lipid droplets serve as potential sources of substrates for VLDL secretion. However, the regulatory mechanisms linking these two processes remain poorly understood. Here, we identify SEC16B, a scaffold protein localized at the ER exit sites (ERES), as a key regulator of hepatic lipid secretion and storage. Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) in SEC16B to be highly related to plasma lipid levels in humans. In mice, hepatic Sec16b deficiency reduces serum lipid levels by impairing MTP-independent VLDL lipidation and disrupting COPII-mediated intracellular trafficking. Additionally, SEC16B partially localizes at ER-lipid droplet contact sites, where it promotes lipid droplet expansion by facilitating the recruitment of ER proteins to lipid droplets. More importantly, Sec16b deletion significantly lowers serum lipids and decreases atherosclerotic lesion size in Ldlr null mice. Taken together, these findings uncover a novel mechanism coordinating VLDL and lipid droplet metabolism and highlight SEC16B as a promising therapeutic target for atherosclerosis."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Novel regulation of hepatic lipid secretion and storage"]}]}],"canonical_facts":{"dc:contributor":["Wang, Bo","Nelson, Erik","Spinella, Michael J","Yang, Jing"],"dc:creator":["Lu, Wei"],"dc:date":["2025-04-15","2025-05"],"dc:description":["Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2027-05-01","The student, Wei Lu, accepted the attached license on 2025-04-14 at 11:41.","The student, Wei Lu, submitted this Dissertation for approval on 2025-04-14 at 11:54.","This Dissertation was approved for publication on 2025-04-15 at 16:42.","DSpace SAF Submission Ingestion Package generated from Vireo submission #21764 on 2025-10-19 at 19:52:50","The liver plays a critical role in lipid homeostasis, where lipids are either secreted as very-low-density lipoproteins (VLDL) or stored in lipid droplets. Previous studies have demonstrated a close relationship between VLDL and lipid droplet metabolism. Impaired VLDL secretion has been associated with increased lipid droplet formation, whereas lipid droplets serve as potential sources of substrates for VLDL secretion. However, the regulatory mechanisms linking these two processes remain poorly understood. Here, we identify SEC16B, a scaffold protein localized at the ER exit sites (ERES), as a key regulator of hepatic lipid secretion and storage. Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) in SEC16B to be highly related to plasma lipid levels in humans. In mice, hepatic Sec16b deficiency reduces serum lipid levels by impairing MTP-independent VLDL lipidation and disrupting COPII-mediated intracellular trafficking. Additionally, SEC16B partially localizes at ER-lipid droplet contact sites, where it promotes lipid droplet expansion by facilitating the recruitment of ER proteins to lipid droplets. More importantly, Sec16b deletion significantly lowers serum lipids and decreases atherosclerotic lesion size in Ldlr null mice. Taken together, these findings uncover a novel mechanism coordinating VLDL and lipid droplet metabolism and highlight SEC16B as a promising therapeutic target for atherosclerosis."],"dc:format":["application/pdf"],"dc:identifier":["https://hdl.handle.net/2142/129686"],"dc:language":["en","eng"],"dc:rights":["Copyright 2025 Wei Lu"],"dc:subject":["Atherosclerosis","VLDL","ApoB lipidation","lipid droplet expansion"],"dc:title":["Novel regulation of hepatic lipid secretion and storage"],"dc:type":["text","Thesis"],"thesis:degree_discipline":["VMS - Comparative Biosciences"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois Urbana-Champaign"]},"updated_at":"2026-07-22T22:25:05Z"}