Cited by 231Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismCardiovascular Disease and Adiposity

Diet Induction of Monocyte Chemoattractant Protein‐1 and its Impact on Obesity

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Chen, Airu, Mumick, Sheena, Zhang, Chunsheng, Lamb, John, Dai, Hongyue, Weingarth, Drew, Mudgett, John, Chen, Howard +3 more·2005·Obesity Research

Abstract

Objective: To examine the effect of a high‐fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein‐1 and −3 (MCP‐1 and MCP‐3) in diet‐induced obesity (DIO) and the effect of a lack of MCP‐1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. Research Methods and Procedures: Obese and lean adipose tissues were profiled for expression changes. The time‐course of MCP‐1 and MCP‐3 expression was examined by reverse transcriptase‐polymerase chain reaction. Plasma MCP‐1 levels were determined by enzyme‐linked immunosorbent assay (ELISA). Chemokine receptor‐2 (CCR2) knockout mice were placed on the high‐fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. Results: DIO elevated adipose expression of many inflammatory genes, including MCP‐1 and MCP‐3. Adipose MCP‐1 and MCP‐3 mRNA levels increased within 7 days of starting a high‐fat diet, with elevation of plasma MCP‐1 detected after 4 weeks on the diet. The induction of MCP‐1 and MCP‐3 expression preceded that of tumor necrosis factor‐α. The elevated plasma MCP‐1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP‐1 receptor CCR2. Discussion: A high‐fat diet elevated adipose expression of inflammatory genes, including early induction of MCP‐1 and MCP‐3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP‐1 in obesity, disruption of MCP‐1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.

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  1. Warne JP. Tumor necrosis factor-␣, a key regulator of adi- pose tissue mass. J Endocrinol. 2003;177:351-5.

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Authors
Chen, A., Mumick, S., Zhang, C., Lamb, J., Dai, H., Weingarth, D., Mudgett, J., Chen, H., MacNeil, D. J., Reitman, M. L., & Qian, S.
Affiliations
Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
Corresponding author
Qian, Su
Venue
Obesity Research
Publisher
Wiley
Published
2005-08
Volume
13
Issue
8
Pages
1311-1320
ISSN
  • 1071-7323 (ISSN-L)
  • 1550-8528
OpenAlex
W1973259074
Cited by
231
References
26
Citations by year
2025: 2 · 2024: 9 · 2023: 5 · 2022: 10 · 2021: 7 · 2020: 9 · 2019: 8 · 2018: 8 · 2017: 7 · 2016: 12 · 2015: 12 · 2014: 9 · 2013: 22 · 2012: 15
FWCI
12.19
Type
journal article
Language
en
Open access
Locations
  • Obesity Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords
diet-induced obesity, MCP-1, MCP-3, adipose tissue inflammation, chemokine expression, CCR2 knockout mice, TNF-α, AM251, high-fat diet, systemic inflammation
MeSH terms
CD68 Molecule, Animals, Dietary Fats, Macrophages, Male, Mice, Inbred C57BL, Obesity, RNA, Messenger, Tumor Necrosis Factor-alpha, Antigens, Differentiation, Myelomonocytic, Signal Transduction, Antigens, CD, Adipocytes, Mice, Knockout, Inflammation Mediators, Chemokine CCL2, Receptors, Chemokine, Gene Expression Profiling, Carboxypeptidases A, Mice, Receptors, CCR2

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