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Obesity Studies

Aberrant Accumulation of Undifferentiated Myeloid Cells in the Adipose Tissue of CCR2-Deficient Mice Delays Improvements in Insulin Sensitivity

  1. Dario A. Gutierrez,
  2. Arion Kennedy,
  3. Jeb S. Orr,
  4. Emily K. Anderson,
  5. Corey D. Webb,
  6. William K. Gerrald and
  7. Alyssa H. Hasty⇓
  1. Department of Molecular Physiology and Biophysics, Vanderbilt School of Medicine, Nashville, Tennessee
  1. Corresponding author: Alyssa H. Hasty, alyssa.hasty{at}vanderbilt.edu.
Diabetes 2011 Nov; 60(11): 2820-2829. https://doi.org/10.2337/db11-0314
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  • Correction - May 01, 2012

Abstract

OBJECTIVE Mice with CCR2 deficiency are protected from insulin resistance but only after long periods of high-fat diet (HFD) feeding, despite the virtual absence of circulating inflammatory monocytes. We performed a time course study in mice with hematopoietic and global CCR2 deficiency to determine adipose tissue–specific mechanisms for the delayed impact of CCR2 deficiency on insulin resistance.

RESEARCH DESIGN AND METHODS Mice with global or hematopoietic CCR2 deficiency (CCR2−/− and BM-CCR2−/−, respectively) and wild-type controls (CCR2+/+ and BM-CCR2+/+, respectively) were placed on an HFD for 6, 12, and 20 weeks. Adipose tissue myeloid populations, degree of inflammation, glucose tolerance, and insulin sensitivity were assessed.

RESULTS Flow cytometry analysis showed that two different populations of F4/80+ myeloid cells (CD11bloF4/80lo and CD11bhiF4/80hi) accumulated in the adipose tissue of CCR2−/− and BM-CCR2−/− mice after 6 and 12 weeks of HFD feeding, whereas only the CD11bhiF4/80hi population was detected in the CCR2+/+ and BM-CCR2+/+ controls. After 20 weeks of HFD feeding, the CD11bloF4/80lo cells were no longer present in the adipose tissue of CCR2−/− mice, and only then were improvements in adipose tissue inflammation detected. Gene expression and histological analysis of the CD11bloF4/80lo cells indicated that they are a unique undifferentiated monocytic inflammatory population. The CD11bloF4/80lo cells are transiently found in wild-type mice, but CCR2 deficiency leads to the aberrant accumulation of these cells in adipose tissue.

CONCLUSIONS The discovery of this novel adipose tissue monocytic cell population provides advances toward understanding the pleiotropic role of CCR2 in monocyte/macrophage accumulation and regulation of adipose tissue inflammation.

Footnotes

  • This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db11-0314/-/DC1.

  • Received March 8, 2011.
  • Accepted July 31, 2011.
  • © 2011 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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Aberrant Accumulation of Undifferentiated Myeloid Cells in the Adipose Tissue of CCR2-Deficient Mice Delays Improvements in Insulin Sensitivity
Dario A. Gutierrez, Arion Kennedy, Jeb S. Orr, Emily K. Anderson, Corey D. Webb, William K. Gerrald, Alyssa H. Hasty
Diabetes Nov 2011, 60 (11) 2820-2829; DOI: 10.2337/db11-0314

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Aberrant Accumulation of Undifferentiated Myeloid Cells in the Adipose Tissue of CCR2-Deficient Mice Delays Improvements in Insulin Sensitivity
Dario A. Gutierrez, Arion Kennedy, Jeb S. Orr, Emily K. Anderson, Corey D. Webb, William K. Gerrald, Alyssa H. Hasty
Diabetes Nov 2011, 60 (11) 2820-2829; DOI: 10.2337/db11-0314
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