Evidence map›Paper›PMID 26620890›Full record

ArticleInternational journal of obesity (2005)2016

Role of MCP-1 on inflammatory processes and metabolic dysfunction following high-fat feedings in the FVB/N strain.

T L Cranford, R T Enos, K T Velázquez, J L McClellan, J M Davis, U P Singh, M Nagarkatti, P S Nagarkatti, C M Robinson, E A Murphy

Open access · greenAbstract read
In one paragraph

Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  17. Antiobesity Effect ofEvidence-based complementary and alternative medicine : eCAM · 2023
    Article
  18. Article
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  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

10 authors at 2 institutions in 1 country.

T L CranfordDepartment of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC, USA.
R T EnosDepartment of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC, USA.
K T VelázquezDepartment of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC, USA.
J L McClellanDepartment of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC, USA.
J M DavisDepartment of Exercise Science, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA.
U P SinghDepartment of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC, USA.
M NagarkattiDepartment of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC, USA.
P S NagarkattiDepartment of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC, USA.
C M RobinsonDepartment of Biomedical Sciences, West Virginia School of Osteopathic Medicine, Lewisburg, WV, USA.
E A MurphyDepartment of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC, USA.
University of South Carolina · USWest Virginia School of Osteopathic Medicine · US

Funding

Targeting early ceramide elevation in pre-symptomatic eczemaP20GM103641 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ENOS, REILLY, NAGARKATTI, PRAKASH S · 2012 to 2023
$20.7M
Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
Regulation of Macrophages in Obesity-Enhanced Colon Cancer:Benefits of QuercetinK01AT007824 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI MURPHY, ELIZABETH ANGELA · 2013 to 2017
$632k
Macrophages in High Fat Diet Enhanced Colorectal Cancer: Regulation by miRNA-155R21CA167058 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI MURPHY, ELIZABETH ANGELA · 2013 to 2014
$323k
Regulation of Macrophages by miRNA-155 in Colon Cancer: Benefits of QuercetinR21CA175636 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI MURPHY, ELIZABETH ANGELA · 2014 to 2015
$304k
Regulation of Macrophages in Obesity-Enhanced Breast CancerF31CA183458 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI CRANFORD, TARYN LINDSEY · 2014 to 2016
$85k
NCCIH NIH HHS K01 AT007824NCCIH NIH HHS P01 AT003961NCI NIH HHS F31 CA183458NCI NIH HHS R21 CA167058NCI NIH HHS R21 CA175636NIGMS NIH HHS P20 GM103641
6 · The paper itself

Abstract

backgroundMonocyte chemoattractant protein 1 (MCP-1) is known to be an important chemokine for macrophage recruitment. Thus, targeting MCP-1 may prevent the perturbations associated with macrophage-induced inflammation in adipose tissue. However, inconsistencies in the available animal literature have questioned the role of this chemokine in this process. The purpose of this study was to examine the role of MCP-1 on obesity-related pathologies.

methodsWild-type and MCP-1-deficient mice on an friend virus B NIH (FVB/N) background were assigned to either low-fat diet or high-fat diet (HFD) treatment for a period of 16 weeks. Body weight and body composition were measured weekly and monthly, respectively. Fasting blood glucose and insulin, and glucose tolerance were measured at 16 weeks. Macrophages, T-cell markers, inflammatory mediators and markers of fibrosis were examined in the adipose tissue at the time of killing the mice.

resultsAs expected, HFD increased adiposity (body weight, fat mass, fat percent and adipocyte size), metabolic dysfunction (impaired glucose metabolism and insulin resistance) macrophage number (CD11b(+)F480(+) cells, and gene expression of EMR1 and CD11c), T-cell markers (gene expression of CD4 and CD8), inflammatory mediators (pNFκB and pJNK, and mRNA expression of MCP-1, CCL5, C-X-C motif chemokine-14, tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6)) and fibrosis (expression of IL-10, IL-13, TGF-β and matrix metalloproteinase-2 (MMP2); P<0.05). However, contrary to our hypothesis, MCP-1 deficiency exacerbated many of these responses resulting in a further increase in adiposity (body weight, fat mass, fat percent and adipocyte size), metabolic dysregulation, macrophage markers (EMR1), inflammatory cell infiltration and fibrosis (formation of type I and III collagens, mRNA expression of IL-10 and MMP2; P<0.05).

conclusionsThese data suggest that MCP-1 may be a necessary component of the inflammatory response required for adipose tissue protection, remodeling and healthy expansion in the FVB/N strain in response to HFD feedings.

Indexed as

Diet, High-FatAdipose TissueAnimalsChemokine CCL2Disease Models, AnimalGene Expression ProfilingImmunohistochemistryInflammationInsulin ResistanceMacrophagesMaleMiceMice, Inbred C57BLObesityTumor Necrosis Factor-alphaCcl2 protein, mouseChemokine CCL2Tumor Necrosis Factor-alpha

Identifiers

PMID26620890
PMCPMC4854829
OpenAlexW2199056716

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.