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Intestinal Nogo-B reduces GLP1 levels by binding to proglucagon on the endoplasmic reticulum to inhibit PCSK1 cleavage.

التفاصيل البيبلوغرافية
العنوان: Intestinal Nogo-B reduces GLP1 levels by binding to proglucagon on the endoplasmic reticulum to inhibit PCSK1 cleavage.
المؤلفون: Gong K; Division of Life Sciences and Medicine, Department of Cardiology, the First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China.; Department of Physiology, Faculty of Basic Medical Sciences, Hubei Key Laboratory of Embryonic Stem Cell Research, Hubei University of Medicine, Shiyan, Hubei, China.; Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, Hefei University of Technology, Hefei, Anhui, China., Xue C; College of Life Sciences, Key Laboratory of Bioactive Materials of Ministry of Education, Nankai University, Tianjin, China., Feng Z; Division of Life Sciences and Medicine, Department of Cardiology, the First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China., Pan R; Division of Life Sciences and Medicine, Department of Cardiology, the First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China., Wang M; Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, Hefei University of Technology, Hefei, Anhui, China., Chen S; Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, Hefei University of Technology, Hefei, Anhui, China., Chen Y; Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, Hefei University of Technology, Hefei, Anhui, China., Guan Y; Department of Geriatrics, and Shenzhen Clinical Research Centre for Geriatrics, Shenzhen People's Hospital, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, Guangdong, China., Dai L; Department of Geriatrics, and Shenzhen Clinical Research Centre for Geriatrics, Shenzhen People's Hospital, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, Guangdong, China., Zhang S; Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, Hefei University of Technology, Hefei, Anhui, China., Jiang L; Laboratory of Immunoengineering, Institute of Health and Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, Anhui, China., Li L; Laboratory of Immunoengineering, Institute of Health and Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, Anhui, China., Wang B; Department of Pathology, China-Japan Friendship Hospital, Beijing, China., Yin Z; Division of Life Sciences and Medicine, Department of Cardiology, the First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China., Ma L; Division of Life Sciences and Medicine, Department of Cardiology, the First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China., Iwakiri Y; Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT, USA., Tang J; Department of Physiology, Faculty of Basic Medical Sciences, Hubei Key Laboratory of Embryonic Stem Cell Research, Hubei University of Medicine, Shiyan, Hubei, China., Liao C; Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, Hefei University of Technology, Hefei, Anhui, China., Chen H; Department of Biochemistry & Molecular Biology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China., Duan Y; Division of Life Sciences and Medicine, Department of Cardiology, the First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China. yajunduan@ustc.edu.cn.
المصدر: Nature communications [Nat Commun] 2024 Aug 10; Vol. 15 (1), pp. 6845. Date of Electronic Publication: 2024 Aug 10.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Diabetes Mellitus, Type 2*/metabolism , Diabetes Mellitus, Type 2*/genetics , Endoplasmic Reticulum*/metabolism , Glucagon-Like Peptide 1*/metabolism , Nogo Proteins*/metabolism , Nogo Proteins*/genetics , Proglucagon*/metabolism , Proglucagon*/genetics , Proprotein Convertase 1*/metabolism , Proprotein Convertase 1*/genetics, Animals ; Humans ; Male ; Mice ; Enteroendocrine Cells/metabolism ; Golgi Apparatus/metabolism ; HEK293 Cells ; Insulin/metabolism ; Insulin Resistance ; Intestines/pathology ; Mice, Inbred C57BL ; Mice, Knockout ; Protein Binding ; Proteolysis
مستخلص: Glucagon-like peptide 1 (GLP1), which is mainly processed and cleaved from proglucagon in enteroendocrine cells (EECs) of the intestinal tract, acts on the GLP1 receptor in pancreatic cells to stimulate insulin secretion and to inhibit glucagon secretion. However, GLP1 processing is not fully understood. Here, we show that reticulon 4B (Nogo-B), an endoplasmic reticulum (ER)-resident protein, interacts with the major proglucagon fragment of proglucagon to retain proglucagon on the ER, thereby inhibiting PCSK1-mediated cleavage of proglucagon in the Golgi. Intestinal Nogo-B knockout in male type 2 diabetes mellitus (T2DM) mice increases GLP1 and insulin levels and decreases glucagon levels, thereby alleviating pancreatic injury and insulin resistance. Finally, we identify aberrantly elevated Nogo-B expression and inhibited proglucagon cleavage in EECs from diabetic patients. Our study reveals the subcellular regulatory processes involving Nogo-B during GLP1 production and suggests intestinal Nogo-B as a potential therapeutic target for T2DM.
(© 2024. The Author(s).)
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معلومات مُعتمدة: U22A20272 National Natural Science Foundation of China (National Science Foundation of China); 82304503 National Science Foundation of China | Young Scientists Fund; 82300516 National Science Foundation of China | Young Scientists Fund
المشرفين على المادة: 89750-14-1 (Glucagon-Like Peptide 1)
0 (Insulin)
0 (Nogo Proteins)
55963-74-1 (Proglucagon)
EC 3.4.21.93 (Proprotein Convertase 1)
تواريخ الأحداث: Date Created: 20240809 Date Completed: 20240809 Latest Revision: 20240813
رمز التحديث: 20240814
مُعرف محوري في PubMed: PMC11315690
DOI: 10.1038/s41467-024-51352-3
PMID: 39122737
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-024-51352-3