Evidence map›Paper›PMID 31885214›Full record

ArticleEMBO reports2020

DOCK5 regulates energy balance and hepatic insulin sensitivity by targeting mTORC1 signaling.

Yerui Lai, Anjiang Zhao, Minghong Tan, Mengliu Yang, Yao Lin, Shengbing Li, Jinlin Song, Hongting Zheng, Zhiming Zhu, Dongfang Liu and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Signaling pathways in obesity: mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022
    Review
  15. Physical Activity Rewires the Human Brain against Neurodegeneration.International journal of molecular sciences · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Review
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

13 authors at 6 institutions in 2 countries.

Yerui LaiDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Anjiang ZhaoThe Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Minghong TanDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Mengliu YangDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Yao LinThe Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Shengbing LiDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Jinlin SongChongqing Key Laboratory for oral Diseases and Biomedical Science, College of Stomatology, Chongqing Medical University, Chongqing, China.
Hongting ZhengDepartment of Endocrinology, Xinqiao Hospital, Third Military Medical University, Chongqing, China.ORCID 0000-0002-6930-0103
Zhiming ZhuDepartment of Hypertension and Endocrinology, Daping Hospital, Chongqing Institute of Hypertension, Third Military Medical University, Chongqing, China.
Dongfang LiuDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Chaohong LiuDepartment of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.
Ling LiDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.ORCID 0000-0002-0087-3034
Gangyi YangDepartment of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.ORCID 0000-0002-6458-6747
Dalian Medical University · CNArmy Medical University · CNChongqing Medical University · CNHuazhong University of Science and Technology · CNStomatological Hospital of Chongqing Medical University · CNThe University of Queensland · AU

Funding

Chongqing Education Commission and Chongqing Medical University CYB16104Chongqing Education Commission and Chongqing Medical University CYB18159National Natural Science Foundation of China 81601214National Natural Science Foundation of China 81670755National Natural Science Foundation of China 81700758National Natural Science Foundation of China 81873658National Natural Science Foundation of China IRT1216
6 · The paper itself

Abstract

The dedicator of cytokinesis 5 (DOCK5) is associated with obesity. However, the mechanism by which DOCK5 contributes to obesity remains completely unknown. Here, we show that hepatic DOCK5 expression significantly decreases at a state of insulin resistance (IR). Deletion of DOCK5 in mice reduces energy expenditure, promotes obesity, augments IR, dysregulates glucose metabolism, and activates the mTOR (Raptor)/S6K1 pathway under a high-fat diet (HFD). The overexpression of DOCK5 in hepatocytes inhibits gluconeogenic gene expression and increases the level of insulin receptor (InsR) and Akt phosphorylation. DOCK5 overexpression also inhibits mTOR/S6K1 phosphorylation and decreases the level of raptor protein expression. The opposite effects were observed in DOCK5-deficient hepatocytes. Importantly, in liver-specific Raptor knockout mice and associated hepatocytes, the effects of an adeno-associated virus (AAV8)- or adenovirus-mediated DOCK5 knockdown on glucose metabolism and insulin signaling are largely eliminated. Additionally, DOCK5-Raptor interaction is indispensable for the DOCK5-mediated regulation of hepatic glucose production (HGP). Therefore, DOCK5 acts as a regulator of Raptor to control hepatic insulin activity and glucose homeostasis.

Indexed as

Insulin ResistanceAnimalsDiet, High-FatEnergy MetabolismGuanine Nucleotide Exchange FactorsInsulinLiverMiceMice, Inbred C57BLSignal TransductionDock5 protein, mouseGuanine Nucleotide Exchange FactorsInsulinDOCK5glucose metabolisminsulin resistancemTOR pathway

Identifiers

PMID31885214
PMCPMC7001503
OpenAlexW2997593080

What OpenQuestion 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 OpenQuestion graph.