Evidence map›Paper›PMID 24770415›Full record

ArticleThe Journal of biological chemistry2014

Myeloid cell-specific disruption of Period1 and Period2 exacerbates diet-induced inflammation and insulin resistance.

Hang Xu, Honggui Li, Shih-Lung Woo, Sam-Moon Kim, Vikram R Shende, Nichole Neuendorff, Xin Guo, Ting Guo, Ting Qi, Ya Pei and 9 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

64 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
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  6. Chrononutrition: Potential, Challenges, and Application in Managing Obesity.International journal of molecular sciences · 2025
    Review
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  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
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  15. Review
  16. Article
  17. Article
  18. Circadian Regulation of Macrophages and Osteoclasts in Rheumatoid Arthritis.International journal of molecular sciences · 2023
    Review
  19. Review
  20. Article

4 more citing papers are in PubMed but not listed here.

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

19 authors at 5 institutions in 2 countries.

Hang XuFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843.
Honggui LiFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843.
Shih-Lung WooFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843.
Sam-Moon KimDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M Health Science Center, Bryan, Texas 77807.
Vikram R ShendeDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M Health Science Center, Bryan, Texas 77807.
Nichole NeuendorffDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M Health Science Center, Bryan, Texas 77807.
Xin GuoFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843.
Ting GuoFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843.
Ting QiFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843.
Ya PeiFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843.
Yan ZhaoFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843.
Xiang HuFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843, Department of Endocrinology and.
Jiajia ZhaoFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843, Department of Stomatology, Union Hospital, Tongji College of Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China, and.
Lili ChenDepartment of Stomatology, Union Hospital, Tongji College of Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China, and.
Lulu ChenDepartment of Endocrinology and.
Jun-Yuan JiDepartment of Molecular and Cellular Medicine and.
Robert C AlanizDepartment of Microbial and Molecular Pathogenesis, College of Medicine, Texas A&M Health Science Center, College Station, Texas 77843.
David J EarnestDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M Health Science Center, Bryan, Texas 77807, DEARNEST@medicine.tamhsc.edu.
Chaodong WuFrom the Department of Nutrition and Food Science, Texas A&M University, College Station, Texas 77843, cdwu@tamu.edu.
Texas A&M University · USTexas A&M Health Science Center · USCellular Research (United States) · USHuazhong University of Science and Technology · CNUnion Hospital · CN

Funding

Protective role of adenosine 2A receptor in NAFLDR01DK095862 · NIDDK · TEXAS A&M AGRILIFE RESEARCH · PI WU, CHAODONG · 2013 to 2017
$1.6M
Context-specific Functions of CDK8R01DK095013 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI JI, JUN-YUAN · 2013 to 2017
$1.5M
Metabolic regulation of adipocyte-macrophage crosstalk in obesityR01DK095828 · NIDDK · TEXAS A&M AGRILIFE RESEARCH · PI WU, CHAODONG · 2013 to 2016
$1.3M
NIDDK NIH HHS 1R01DK095828NIDDK NIH HHS 1R01DK095862NIDDK NIH HHS R01 DK095013NIDDK NIH HHS R01 DK095828NIDDK NIH HHS R01 DK095862
6 · The paper itself

Abstract

The circadian clockworks gate macrophage inflammatory responses. Given the association between clock dysregulation and metabolic disorders, we conducted experiments to determine the extent to which over-nutrition modulates macrophage clock function and whether macrophage circadian dysregulation is a key factor linking over-nutrition to macrophage proinflammatory activation, adipose tissue inflammation, and systemic insulin resistance. Our results demonstrate that 1) macrophages from high fat diet-fed mice are marked by dysregulation of the molecular clockworks in conjunction with increased proinflammatory activation, 2) global disruption of the clock genes Period1 (Per1) and Per2 recapitulates this amplified macrophage proinflammatory activation, 3) adoptive transfer of Per1/2-disrupted bone marrow cells into wild-type mice potentiates high fat diet-induced adipose and liver tissue inflammation and systemic insulin resistance, and 4) Per1/2-disrupted macrophages similarly exacerbate inflammatory responses and decrease insulin sensitivity in co-cultured adipocytes in vitro. Furthermore, PPARγ levels are decreased in Per1/2-disrupted macrophages and PPARγ2 overexpression ameliorates Per1/2 disruption-associated macrophage proinflammatory activation, suggesting that this transcription factor may link the molecular clockworks to signaling pathways regulating macrophage polarization. Thus, macrophage circadian clock dysregulation is a key process in the physiological cascade by which diet-induced obesity triggers macrophage proinflammatory activation, adipose tissue inflammation, and insulin resistance.

Indexed as

Diet, High-FatInsulin ResistanceAdipocytesAnimalsBone Marrow CellsCoculture TechniquesInflammationMacrophagesMiceMice, Inbred C57BLPeriod Circadian ProteinsPPAR gammaPer1 protein, mousePer2 protein, mousePeriod Circadian ProteinsPPAR gammaAdipose TissueCircadian ClockInflammationInsulin ResistanceMacrophage

Identifiers

PMID24770415
PMCPMC4047405
OpenAlexW2058784630

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.