Evidence map›Paper›PMID 40586350›Full record

ArticleAdipocyte2025

Electroacupuncture stimulation induced M1/M2 polarization in white adipose tissues by activating the Y1 receptor in obese mice to reduce chronic inflammation.

Mengjiang Lu, Ziwei Yu, Xingyu Yang, Ze Yang, Tiancheng Xu, Zhi Yu, Xinyue Jing, Li An, Jianbin Zhang, Bin Xu

Abstract read
In one paragraph

Article in Adipocyte, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
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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

10 authors.

Mengjiang LuKey Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.
Ziwei YuKey Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.
Xingyu YangKey Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.
Ze YangKey Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.
Tiancheng XuKey Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.
Zhi YuKey Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.
Xinyue JingKey Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.
Li AnSchool of Traditional Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Jianbin ZhangDepartment of Acupuncture and Moxibustion, Jiangsu Second Hospital of Chinese Medicine, Nanjing, China.
Bin XuKey Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation in obesity can induce complications such as diabetes and cardiovascular disease. Visceral adipose tissue is the main source of inflammation, but it is difficult to regulate effectively. Here, we investigated whether ES suppressed inflammation in eWAT and reduced chronic inflammation in obese individuals. We established a high-fat diet (HFD) model with C57BL/6J mice to measure chronic inflammation in obesity. In addition, the sympathetic nerve activity (SNA) was measured with the electrophysiological technique, the immunostaining and flow cytometry were used to detect the Y1 receptors in macrophage. Finally, the key role of the M1/M2 polarization in white adipose tissues by activating the Y1 receptor was verified by Y1 receptor antagonist BIBP3226. ES reduced the contents of IL-1β, TNF-α, IL-6 and TGF-β in the plasma and the mRNA expression of il-1 and tnfα in eWAT. Also, ES suppressed SNA in eWAT which regulated NPY1R receptor. In addition, ES induced M1/M2 polarization in eWAT via the Y1 receptor. The injection of a Y1 receptor (NPY1R) antagonist BIBP3226 restrained M1/M2 polarization. Further studies revealed that ES regulated sympathetic axons in eWAT to activate the Y1 receptor. This research demonstrates ES reduce chronic inflammation e mechanism is associated with the sympathetic Y1 receptor pathway, which promotes M1/M2 polarization.

Indexed as

Adipose Tissue, WhiteElectroacupunctureInflammationObesityReceptors, Neuropeptide YAnimalsDiet, High-FatMacrophagesMaleMiceMice, Inbred C57BLMice, ObeseSympathetic Nervous Systemneuropeptide Y-Y1 receptorReceptors, Neuropeptide YElectroacupunctureM1/M2 polarizationobesityvisceral adipose tissueY1 receptor

Identifiers

PMID40586350
PMCPMC12218457

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.