Evidence map›Paper›PMID 38320300›Full record

ArticleDiabetes2024

Adipocyte-Specific Hnrnpa1 Knockout Aggravates Obesity-Induced Metabolic Dysfunction via Upregulation of CCL2.

Xiaoya Li, Yingying Su, Yiting Xu, Tingting Hu, Xuhong Lu, Jingjing Sun, Wenfei Li, Jian Zhou, Xiaojing Ma, Ying Yang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% of its field
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Xiaoya LiDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.
Yingying SuDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.
Yiting XuDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.
Tingting HuDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.
Xuhong LuDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.
Jingjing SunDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.
Wenfei LiDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.
Jian ZhouDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0002-1534-2279
Xiaojing MaDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0001-9607-161X
Ying YangDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0001-8355-6642
Yuqian BaoDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0002-4754-3470
Shanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China 82200897National Science Foundation of China 82170889Shanghai Research Center for Endocrine and Metabolic Diseases 2022ZZ01002
6 · The paper itself

Abstract

Heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1) is involved in lipid and glucose metabolism via mRNA processing. However, whether and how HNRNPA1 alters adipocyte function in obesity remain obscure. Here, we found that the obese state downregulated HNRNPA1 expression in white adipose tissue (WAT). The depletion of adipocyte HNRNPA1 promoted markedly increased macrophage infiltration and expression of proinflammatory and fibrosis genes in WAT of obese mice, eventually leading to exacerbated insulin sensitivity, glucose tolerance, and hepatic steatosis. Mechanistically, HNRNPA1 interacted with Ccl2 and regulated its mRNA stability. Intraperitoneal injection of CCL2-CCR2 signaling antagonist improved adipose tissue inflammation and systemic glucose homeostasis. Furthermore, HNRNPA1 expression in human WAT was negatively correlated with BMI, fat percentage, and subcutaneous fat area. Among individuals with 1-year metabolic surgery follow-up, HNRNPA1 expression was positively related to percentage of total weight loss. These findings identify adipocyte HNRNPA1 as a link between adipose tissue inflammation and systemic metabolic homeostasis, which might be a promising therapeutic target for obesity-related disorders. ARTICLE HIGHLIGHTS:

Indexed as

Chemokine CCL2Heterogeneous Nuclear Ribonucleoprotein A1Insulin ResistanceObesityAdipocytesAdipose Tissue, WhiteAnimalsGlucoseInflammationMiceMice, Inbred C57BLMice, KnockoutUp-RegulationCcl2 protein, mouseChemokine CCL2GlucoseHeterogeneous Nuclear Ribonucleoprotein A1

Identifiers

PMID38320300
PMCPMC11043064
OpenAlexW4391558356

What Socratic holds

Textmetadata
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.