{"id":4445,"date":"2024-11-07T12:58:37","date_gmt":"2024-11-07T17:58:37","guid":{"rendered":"https:\/\/med.virginia.edu\/physiology-biophysics\/?p=4445"},"modified":"2026-05-22T16:53:03","modified_gmt":"2026-05-22T20:53:03","slug":"ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications","status":"publish","type":"post","link":"https:\/\/med.virginia.edu\/physiology-biophysics\/2024\/11\/07\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\/","title":{"rendered":"Ling Qi, PhD, Lab Discovers Mechanism Linking Cell Protein Degradation to Obesity and Diabetes, research they published in Nature Communications."},"content":{"rendered":"<div class=\"ac-container ac-adaptiveCard\">\n<div class=\"ac-textBlock\">\n<p>Researchers from the Ling Qi Laboratory at UVA have identified the SEL1L-HRD1 protein complex as crucial for regulating leptin receptor turnover, shedding light on the molecular mechanisms behind metabolic disorders. Their study in <em>Nature Communications<\/em> highlights the role of endoplasmic reticulum-associated protein degradation (ERAD) in the hypothalamus, with significant implications for diet-induced obesity (DIO) and type 2 diabetes.<\/p>\n<p>The team found that SEL1L is vital in POMC-expressing neurons, essential for energy balance and appetite regulation. The absence of SEL1L impairs leptin signaling, increasing susceptibility to high-fat diet-induced issues like fatty liver disease, glucose intolerance, and insulin and leptin resistance.<\/p>\n<p>To read more: <a href=\"https:\/\/news.med.virginia.edu\/research\/mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-discovered-by-ling-qi-phd-laboratory\/?j=3509367&amp;sfmc_sub=7193409&amp;l=35_HTML&amp;u=54882901&amp;mid=100026982&amp;jb=1005\" target=\"_blank\" rel=\"noopener\">Medicine in Motion News<\/a><\/p>\n<\/div>\n<\/div>\n","protected":false},"excerpt":{"rendered":"<p>Researchers from the Ling Qi Laboratory at UVA have identified the SEL1L-HRD1 protein complex as crucial for regulating leptin receptor turnover, shedding light on the molecular mechanisms behind metabolic disorders. Their study in Nature Communications highlights the role of endoplasmic reticulum-associated protein degradation (ERAD) in the hypothalamus, with significant implications for diet-induced obesity (DIO) and [&hellip;]<\/p>\n","protected":false},"author":431,"featured_media":4454,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"inline_featured_image":false,"footnotes":"","_links_to":"","_links_to_target":""},"categories":[1],"tags":[67],"class_list":["post-4445","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-uncategorized","tag-intranet"],"acf":false,"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.4 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Ling Qi, PhD, Lab Discovers Mechanism Linking Cell Protein Degradation to Obesity and Diabetes, research they published in Nature Communications. - Molecular Physiology and Biological Physics<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/med.virginia.edu\/physiology-biophysics\/2024\/11\/07\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Ling Qi, PhD, Lab Discovers Mechanism Linking Cell Protein Degradation to Obesity and Diabetes, research they published in Nature Communications. - Molecular Physiology and Biological Physics\" \/>\n<meta property=\"og:description\" content=\"Researchers from the Ling Qi Laboratory at UVA have identified the SEL1L-HRD1 protein complex as crucial for regulating leptin receptor turnover, shedding light on the molecular mechanisms behind metabolic disorders. Their study in Nature Communications highlights the role of endoplasmic reticulum-associated protein degradation (ERAD) in the hypothalamus, with significant implications for diet-induced obesity (DIO) and [&hellip;]\" \/>\n<meta property=\"og:url\" content=\"https:\/\/med.virginia.edu\/physiology-biophysics\/2024\/11\/07\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\/\" \/>\n<meta property=\"og:site_name\" content=\"Molecular Physiology and Biological Physics\" \/>\n<meta property=\"article:published_time\" content=\"2024-11-07T17:58:37+00:00\" \/>\n<meta property=\"article:modified_time\" content=\"2026-05-22T20:53:03+00:00\" \/>\n<meta property=\"og:image\" content=\"https:\/\/med.virginia.edu\/physiology-biophysics\/wp-content\/uploads\/sites\/376\/2024\/11\/MPBP-Blog-Dr.-Ling-Qi.jpg\" \/>\n\t<meta property=\"og:image:width\" content=\"300\" \/>\n\t<meta property=\"og:image:height\" content=\"300\" \/>\n\t<meta property=\"og:image:type\" content=\"image\/jpeg\" \/>\n<meta name=\"author\" content=\"jcn6f@virginia.edu\" \/>\n<meta name=\"twitter:card\" content=\"summary_large_image\" \/>\n<meta name=\"twitter:label1\" content=\"Written by\" \/>\n\t<meta name=\"twitter:data1\" content=\"jcn6f@virginia.edu\" \/>\n\t<meta name=\"twitter:label2\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data2\" content=\"1 minute\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"Article\",\"@id\":\"https:\\\/\\\/med.virginia.edu\\\/physiology-biophysics\\\/2024\\\/11\\\/07\\\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\\\/#article\",\"isPartOf\":{\"@id\":\"https:\\\/\\\/med.virginia.edu\\\/physiology-biophysics\\\/2024\\\/11\\\/07\\\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\\\/\"},\"author\":{\"name\":\"jcn6f@virginia.edu\",\"@id\":\"https:\\\/\\\/med.virginia.edu\\\/physiology-biophysics\\\/#\\\/schema\\\/person\\\/b04fd9ea0cc1b737c601a7aee39c928c\"},\"headline\":\"Ling Qi, PhD, Lab Discovers Mechanism Linking Cell Protein Degradation to Obesity and Diabetes, research they published in Nature Communications.\",\"datePublished\":\"2024-11-07T17:58:37+00:00\",\"dateModified\":\"2026-05-22T20:53:03+00:00\",\"mainEntityOfPage\":{\"@id\":\"https:\\\/\\\/med.virginia.edu\\\/physiology-biophysics\\\/2024\\\/11\\\/07\\\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\\\/\"},\"wordCount\":128,\"image\":{\"@id\":\"https:\\\/\\\/med.virginia.edu\\\/physiology-biophysics\\\/2024\\\/11\\\/07\\\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\\\/#primaryimage\"},\"thumbnailUrl\":\"https:\\\/\\\/med.virginia.edu\\\/physiology-biophysics\\\/wp-content\\\/uploads\\\/sites\\\/376\\\/2024\\\/11\\\/MPBP-Blog-Dr.-Ling-Qi.jpg\",\"keywords\":[\"Intranet\"],\"inLanguage\":\"en-US\"},{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/med.virginia.edu\\\/physiology-biophysics\\\/2024\\\/11\\\/07\\\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\\\/\",\"url\":\"https:\\\/\\\/med.virginia.edu\\\/physiology-biophysics\\\/2024\\\/11\\\/07\\\/ling-qi-phd-lab-discovers-mechanism-linking-cell-protein-degradation-to-obesity-and-diabetes-research-they-published-in-nature-communications\\\/\",\"name\":\"Ling Qi, PhD, Lab Discovers Mechanism Linking Cell Protein Degradation to Obesity and Diabetes, research they published in Nature Communications. - 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