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Cell Metab. 2016 Jan 12;23(1):165-78. doi: 10.1016/j.cmet.2015.10.003. Epub 2015 Nov 5.

Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance.

Author information

1
Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA 94143, USA.
2
Department of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.
3
Department of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.
4
Department of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA; Howard Hughes Medical Institute, University of California Los Angeles, Los Angeles, CA 90095, USA.
5
Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA 94143, USA; Departments of Physiology and Medicine, University of California San Francisco, San Francisco, CA 94143, USA. Electronic address: ajay.chawla@ucsf.edu.

Erratum in

  • Cell Metab. 2016 Feb 9;23(2):386. Tonotonoz, Peter [corrected to Tontonoz, Peter].

Abstract

Chronic, low-grade inflammation triggered by excess intake of dietary lipids has been proposed to contribute to the pathogenesis of metabolic disorders, such as obesity, insulin resistance, type 2 diabetes, and atherosclerosis. Although considerable evidence supports a causal association between inflammation and metabolic diseases, most tests of this link have been performed in cold-stressed mice that are housed below their thermoneutral zone. We report here that thermoneutral housing of mice has a profound effect on the development of metabolic inflammation, insulin resistance, and atherosclerosis. Mice housed at thermoneutrality develop metabolic inflammation in adipose tissue and in the vasculature at an accelerated rate. Unexpectedly, this increased inflammatory response contributes to the progression of atherosclerosis but not insulin resistance. These findings not only suggest that metabolic inflammation can be uncoupled from obesity-associated insulin resistance, but also point to how thermal stress might limit our ability to faithfully model human diseases in mice.

PMID:
26549485
PMCID:
PMC4715491
DOI:
10.1016/j.cmet.2015.10.003
[Indexed for MEDLINE]
Free PMC Article

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