Evidence map›Paper›PMID 35017472›Full record

ArticleNature communications2022

A propolis-derived small molecule ameliorates metabolic syndrome in obese mice by targeting the CREB/CRTC2 transcriptional complex.

Yaqiong Chen, Jiang Wang, Yibing Wang, Pengfei Wang, Zan Zhou, Rong Wu, Qian Xu, Hanyun You, Yaxin Liu, Lei Wang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
5.0field-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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Phytocompounds That Target White Adipose Tissue for Weight Loss: A Review Spanning From Ucp1 Induction in Rodents to Human Clinical Trials.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Anti-Obesity Effects ofFood science & nutrition · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Biological functions of CRTC2 and its role in metabolism-related diseases.Journal of cell communication and signaling · 2023
    Review
  18. Article
  19. Review
  20. 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

15 authors at 6 institutions in 1 country.

Yaqiong Chen *Key Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Jiang Wang *State Key Laboratory of Drug Research and CAS Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.ORCID http://orcid.org/0000-0003-1705-4905
Yibing WangState Key Laboratory of Drug Research and CAS Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Pengfei WangUniversity of Chinese Academy of Sciences, No.19A Yuquan Road, 100049, Beijing, China.
Zan ZhouUniversity of Chinese Academy of Sciences, No.19A Yuquan Road, 100049, Beijing, China.
Rong WuUniversity of Chinese Academy of Sciences, No.19A Yuquan Road, 100049, Beijing, China.
Qian XuDepartment of Endocrinology, the First Affiliated Hospital of Harbin Medical University, 150081, Heilongjiang Province, China.
Hanyun YouJiangsu Key Laboratory for Functional Substance of Chinese Medicine, School of Pharmacy, Nanjing University of Chinese Medicine, 210023, Nanjing, China.
Yaxin LiuKey Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Lei WangKey Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Lingqin ZhouKey Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Yuting WuKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, 200031, Shanghai, China.
Lihong HuJiangsu Key Laboratory for Functional Substance of Chinese Medicine, School of Pharmacy, Nanjing University of Chinese Medicine, 210023, Nanjing, China. lhhu@njucm.edu.cn.
Hong LiuState Key Laboratory of Drug Research and CAS Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China. hliu@simm.ac.cn.ORCID http://orcid.org/0000-0003-3685-6268
Yi LiuKey Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China. liuyee@fudan.edu.cn.ORCID http://orcid.org/0000-0002-6889-4608
Shanghai Institutes for Biological Sciences · CNChinese Academy of Sciences · CNFudan University · CNNanjing University of Chinese Medicine · CNShanghai Medical College of Fudan University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular targets and mechanisms of propolis ameliorating metabolic syndrome are not fully understood. Here, we report that Brazilian green propolis reduces fasting blood glucose levels in obese mice by disrupting the formation of CREB/CRTC2 transcriptional complex, a key regulator of hepatic gluconeogenesis. Using a mammalian two-hybrid system based on CREB-CRTC2, we identify artepillin C (APC) from propolis as an inhibitor of CREB-CRTC2 interaction. Without apparent toxicity, APC protects mice from high fat diet-induced obesity, decreases fasting glucose levels, enhances insulin sensitivity and reduces lipid levels in the serum and liver by suppressing CREB/CRTC2-mediated both gluconeogenic and SREBP transcriptions. To develop more potential drugs from APC, we designed and found a novel compound, A57 that exhibits higher inhibitory activity on CREB-CRTC2 association and better capability of improving insulin sensitivity in obese animals, as compared with APC. In this work, our results indicate that CREB/CRTC2 is a suitable target for developing anti-metabolic syndrome drugs.

Indexed as

Drug Delivery SystemsAnimalsBlood GlucoseBrazilCREB-Binding ProteinDrug DevelopmentDrug DiscoveryGluconeogenesisInsulin ResistanceLiverMetabolic SyndromeMiceMice, Inbred C57BLMice, Inbred ICRMice, ObeseObesityBlood GlucoseCREB-Binding ProteinCrebbp protein, mouseCrtc2 protein, mousePropolisTranscription Factors

Identifiers

PMID35017472
PMCPMC8752738
OpenAlexW4206316110

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.