Evidence map›Paper›PMID 42106023›Full record

ArticleMediators of inflammation2026

C1q/TNF-Related Protein 4 (C1QTNF4) Acts as an Adipokine That Ameliorates Diet-Induced Obesity by Improving Energy Metabolism and Alleviating Adipose Inflammation.

Daxiang Na, Yanwei He, Xinrui Liu, Mingjun Huang, Shuo Xie, Hexin Li, Jingying Liu, Hong Zhang, Lu Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Daxiang NaSchool of Basic Medical Sciences, Peking University Health Science Center, Peking University, Beijing, 100191, China, pku.edu.cn.
Yanwei HeSchool of Basic Medical Sciences, Peking University Health Science Center, Peking University, Beijing, 100191, China, pku.edu.cn.ORCID https://orcid.org/0009-0009-2426-2228
Xinrui LiuSchool of Basic Medical Sciences, Peking University Health Science Center, Peking University, Beijing, 100191, China, pku.edu.cn.
Mingjun HuangSchool of Basic Medical Sciences, Peking University Health Science Center, Peking University, Beijing, 100191, China, pku.edu.cn.
Shuo XieSchool of Basic Medical Sciences, Peking University Health Science Center, Peking University, Beijing, 100191, China, pku.edu.cn.
Hexin LiBiological Sample Management Center, Beijing Hospital, Beijing, 100730, China, bjhmoh.cn.
Jingying LiuSchool of Basic Medical Sciences, Peking University Health Science Center, Peking University, Beijing, 100191, China, pku.edu.cn.
Hong ZhangSchool of Basic Medical Sciences, Peking University Health Science Center, Peking University, Beijing, 100191, China, pku.edu.cn.ORCID https://orcid.org/0000-0001-6290-2454
Lu WangSchool of Basic Medical Sciences, Peking University Health Science Center, Peking University, Beijing, 100191, China, pku.edu.cn.ORCID https://orcid.org/0000-0003-0835-0198

Funding

Chinese Academy of Medical Sciences Innovation 2018-I2M-1-002Interdisciplinary Medicine Seed Fund of Peking University BMU2017MX003National Key Research and Development Program of China 2022YFA1104800National Natural Science Foundation of China 81172001National Natural Science Foundation of China 91129707Science and Technology Plan of Beijing City Z211100002921014
6 · The paper itself

Abstract

backgroundThe C1q/TNF-related protein (C1QTNF) plays a crucial role in the intricate connection between obesity and inflammation, acting as a significant adipokine. This study aims to investigate the potential of C1QTNF4 as an antiobesity and anti-inflammatory adipokine.

methodsForty-eight subjects, with or without obesity and diabetes mellitus (DM), were categorized into two groups based on their health condition. Measurements of C1QTNF4, glucose, and adipokine concentrations were conducted. Seven-week-old C57BL/6J mice were segregated into four groups, with eight mice in each group of both sexes. C1QTNF4 transgenic (Tg) mice and their corresponding littermate controls were subjected to either a high-fat (HF) diet (HFD) or a standard chow diet for 14 weeks.

resultsC1QTNF4 and leptin levels increased, while adiponectin levels decreased in subjects with obesity and DM compared to normal individuals. C1QTNF4 Tg mice on a HFD exhibited resistance to weight gain, accompanied by an amelioration of insulin resistance (IR). Fatty liver and chronic adipose inflammation were also mitigated. In the liver and skeletal muscle of C1QTNF4 Tg mice, C1QTNF4 activated the AMP-activated protein kinase (AMPK) pathway associated with insulin sensitivity and energy expenditure. Plasma IL-6 decreased in Tg mice on a HFD, indicating that C1QTNF4 alleviates inflammation via the IL-6-JAK1/2-STAT3 pathway.

conclusionsC1QTNF4 emerges as an adipokine with a regulatory role in adipogenesis, addressing energy imbalances and reducing inflammation. This study suggests that C1QTNF4 represents a potential drug target for treating obesity, IR, and inflammation.

Indexed as

AdipokinesAdipose TissueEnergy MetabolismInflammationObesityAdiponectinAnimalsDiet, High-FatFemaleHumansInsulin ResistanceLeptinMaleMiceMice, Inbred C57BLMice, TransgenicAdipokinesAdiponectinLeptinC1QTNF4inflammationmetabolic diseaseobesity

Identifiers

PMID42106023
PMCPMC13157307

What Socratic holds

Textmetadata
LicenceCC BY
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.