Evidence map›Paper›PMID 39674176›Full record

ArticleCell metabolism2025

FcRn-dependent IgG accumulation in adipose tissue unmasks obesity pathophysiology.

Lexiang Yu, Yong Xiao Yang, Zhen Gong, Qianfen Wan, Yifei Du, Qiuzhong Zhou, Yang Xiao, Tarik Zahr, Zhaobin Wang, Zhewei Yu and 13 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Immunoglobulin G in aging and cancer.Frontiers in immunology · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Influence of Weight Loss and Weight Regain on Adipose Tissue Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors.

Lexiang YuNaomi Berrie Diabetes Center, Department of Medicine, Columbia University, New York, NY 10032, USA; Department of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Yong Xiao YangResearch Center for Endocrine and Metabolic Diseases, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen, Guangdong, China.
Zhen GongDepartment of Biochemistry and Molecular Biophysics, Columbia University, New York, NY, USA.
Qianfen WanNaomi Berrie Diabetes Center, Department of Medicine, Columbia University, New York, NY 10032, USA.
Yifei DuMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Qiuzhong ZhouCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.
Yang XiaoDepartment of Biomedical Engineering, Columbia University, New York, NY 10032, USA.
Tarik ZahrNaomi Berrie Diabetes Center, Department of Medicine, Columbia University, New York, NY 10032, USA.
Zhaobin WangDepartment of Biochemistry and Biophysics, School of Basic Medical Sciences, Peking University, Beijing, China.
Zhewei YuDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Kangkang YangKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education, Shandong Provincial Hospital, School of Laboratory Animal & Shandong Laboratory Animal Center, Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong 250021, China; Institute for Genome Engineered Animal Models of Human Diseases, College of Integrative Medicine, National Center of Genetically Engineered Animal Models for International Research, Liaoning Province Key Lab of Genetically Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Jinyang GengKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education, Shandong Provincial Hospital, School of Laboratory Animal & Shandong Laboratory Animal Center, Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong 250021, China; Institute for Genome Engineered Animal Models of Human Diseases, College of Integrative Medicine, National Center of Genetically Engineered Animal Models for International Research, Liaoning Province Key Lab of Genetically Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Susan K FriedDiabetes Obesity and Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Jing LiDepartment of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Rebecca A HaeuslerNaomi Berrie Diabetes Center, Department of Medicine, Columbia University, New York, NY 10032, USA.
Kam W LeongDepartment of Biomedical Engineering, Columbia University, New York, NY 10032, USA.
Lin BaiDepartment of Biochemistry and Biophysics, School of Basic Medical Sciences, Peking University, Beijing, China.
Yingjie WuKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education, Shandong Provincial Hospital, School of Laboratory Animal & Shandong Laboratory Animal Center, Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong 250021, China; Institute for Genome Engineered Animal Models of Human Diseases, College of Integrative Medicine, National Center of Genetically Engineered Animal Models for International Research, Liaoning Province Key Lab of Genetically Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Lei SunCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.
Pan WangResearch Center for Endocrine and Metabolic Diseases, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen, Guangdong, China.
Bao Ting ZhuResearch Center for Endocrine and Metabolic Diseases, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen, Guangdong, China.
Liheng WangInstitute of Cardiovascular Sciences, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China. Electronic address: lihengwang@hsc.pku.edu.cn.
Li QiangDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China. Electronic address: qiang@pku.edu.cn.

Funding

Bile acids and insulin sensitivityR01DK115825 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Rebecca Anne Haeusler · 2018 to 2026
$5.4M
IgG and Adipose Pathological RemodelingR01DK134471 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Anthony W Ferrante · 2023 to 2026
$1.9M
Mouse Metabolic Measurement SystemS10OD032321 · OD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FERRANTE, ANTHONY W · 2022 to 2022
$436k
NIDDK NIH HHS R01 DK115825NIDDK NIH HHS R01 DK134471NIH HHS S10 OD032321
6 · The paper itself

Abstract

Immunoglobulin G (IgG) is traditionally recognized as a plasma protein that neutralizes antigens for immune defense. However, our research demonstrates that IgG predominantly accumulates in adipose tissue during obesity development, triggering insulin resistance and macrophage infiltration. This accumulation is governed by neonatal Fc receptor (FcRn)-dependent recycling, orchestrated in adipose progenitor cells and macrophages during the early and late stages of diet-induced obesity (DIO), respectively. Targeting FcRn abolished IgG accumulation and rectified insulin resistance and metabolic degeneration in DIO. By integrating artificial intelligence (AI) modeling with in vivo and in vitro experimental models, we unexpectedly uncovered an interaction between IgG's Fc-CH3 domain and the insulin receptor's ectodomain. This interaction hinders insulin binding, consequently obstructing insulin signaling and adipocyte functions. These findings unveil adipose IgG accumulation as a driving force in obesity pathophysiology, providing a novel therapeutic strategy to tackle metabolic dysfunctions.

Indexed as

Adipose TissueHistocompatibility Antigens Class IImmunoglobulin GObesityReceptors, FcAdipocytesAnimalsHumansInsulinInsulin ResistanceMacrophagesMaleMiceMice, Inbred C57BLFc receptor, neonatalHistocompatibility Antigens Class IImmunoglobulin GInsulinReceptors, Fcadipose tissue remodelingFcRnIgGinsulin receptorinsulin resistanceobesity

Identifiers

PMID39674176
PMCPMC11885036

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.