Evidence map›Paper›PMID 38167327›Full record

ArticleNature communications2024

Myeloid-derived grancalcin instigates obesity-induced insulin resistance and metabolic inflammation in male mice.

Tian Su, Yue He, Yan Huang, Mingsheng Ye, Qi Guo, Ye Xiao, Guangping Cai, Linyun Chen, Changjun Li, Haiyan Zhou and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

12 citing papers in PubMed, 16 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 2 countries.

Tian Su *Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Yue He *Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Yan HuangEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Mingsheng YeEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Qi GuoEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Ye XiaoEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.ORCID 0000-0002-1318-692X
Guangping CaiEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Linyun ChenEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Changjun LiEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.ORCID 0000-0003-2718-0921
Haiyan ZhouEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China. hyzhou02@csu.edu.cn.ORCID 0000-0002-0868-3606
Xianghang LuoEndocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China. xianghangluo@csu.edu.cn.
Central South University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81900732National Natural Science Foundation of China (National Science Foundation of China) 81930022National Natural Science Foundation of China (National Science Foundation of China) 82120108009National Natural Science Foundation of China (National Science Foundation of China) 92149306
6 · The paper itself

Abstract

The crosstalk between the bone and adipose tissue is known to orchestrate metabolic homeostasis, but the underlying mechanisms are largely unknown. Herein, we find that GCA + (grancalcin) immune cells accumulate in the bone marrow and release a considerable amount of GCA into circulation during obesity. Genetic deletion of Gca in myeloid cells attenuates metabolic dysfunction in obese male mice, whereas injection of recombinant GCA into male mice causes adipose tissue inflammation and insulin resistance. Mechanistically, we found that GCA binds to the Prohibitin-2 (PHB2) receptor on adipocytes and activates the innate and adaptive immune response of adipocytes via the PAK1-NF-κB signaling pathway, thus provoking the infiltration of inflammatory immune cells. Moreover, we show that GCA-neutralizing antibodies improve adipose tissue inflammation and insulin sensitivity in obese male mice. Together, these observations define a mechanism whereby bone marrow factor GCA initiates adipose tissue inflammation and insulin resistance, showing that GCA could be a potential target to treat metainflammation.

Indexed as

Insulin ResistanceAdipocytesAdipose TissueAnimalsInflammationMaleMiceMice, Inbred C57BLObesity

Identifiers

PMID38167327
PMCPMC10762069
OpenAlexW4390499489

What OpenQuestion 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 OpenQuestion graph.