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mice lacking NKT cells but with a complete complement of CD8<sup>+</sup> T-Cells are not protected against the metabolic abnormalities of diet-induced obesity

Mantell, BS and Stefanovic-Racic, M and Yang, X and Dedousis, N and Sipula, IJ and O'Doherty, RM (2011) mice lacking NKT cells but with a complete complement of CD8<sup>+</sup> T-Cells are not protected against the metabolic abnormalities of diet-induced obesity. PLoS ONE, 6 (6).

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Abstract

The contribution of natural killer T (NKT) cells to the pathogenesis of metabolic abnormalities of obesity is controversial. While the combined genetic deletion of NKT and CD8+ T-cells improves glucose tolerance and reduces inflammation, interpretation of these data have been complicated by the recent observation that the deletion of CD8+ T-cells alone reduces obesity-induced inflammation and metabolic dysregulation, leaving the issue of the metabolic effects of NKT cell depletion unresolved. To address this question, CD1d null mice (CD1d-/-), which lack NKT cells but have a full complement of CD8+ T-cells, and littermate wild type controls (WT) on a pure C57BL/6J background were exposed to a high fat diet, and glucose intolerance, insulin resistance, dyslipidemia, inflammation, and obesity were assessed. Food intake (15.5±4.3 vs 15.3±1.8 kcal/mouse/day), weight gain (21.8±1.8 vs 22.8±1.4 g) and fat mass (18.6±1.9 vs 19.5±2.1 g) were similar in CD1d-/- and WT, respectively. As would be expected from these data, metabolic rate (3.0±0.1 vs 2.9±0.2 ml O2/g/h) and activity (21.6±4.3 vs 18.5±2.6 beam breaks/min) were unchanged by NKT cell depletion. Furthermore, the degree of insulin resistance, glucose intolerance, liver steatosis, and adipose and liver inflammatory marker expression (TNFα, IL-6, IL-10, IFN-γ, MCP-1, MIP1α) induced by high fat feeding in CD1d-/- were not different from WT. We conclude that deletion of NKT cells, in the absence of alterations in the CD8+ T-cell population, is insufficient to protect against the development of the metabolic abnormalities of diet-induced obesity. © 2011 Mantell et al.


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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Mantell, BS
Stefanovic-Racic, Mmas31@pitt.eduMAS31
Yang, Xxiy29@pitt.eduXIY29
Dedousis, N
Sipula, IJiansipula@pitt.eduIJSST2
O'Doherty, RMrmo1@pitt.eduRMO1
Contributors:
ContributionContributors NameEmailPitt UsernameORCID
EditorFadini, Gian PaoloUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Date: 10 June 2011
Date Type: Publication
Journal or Publication Title: PLoS ONE
Volume: 6
Number: 6
DOI or Unique Handle: 10.1371/journal.pone.0019831
Schools and Programs: School of Medicine > Microbiology and Molecular Genetics
Refereed: Yes
MeSH Headings: Adiposity--immunology; Animals; Antigens, CD1d--genetics; Antigens, CD1d--metabolism; Biological Markers--metabolism; Body Weight--immunology; CD8-Positive T-Lymphocytes--immunology; CD8-Positive T-Lymphocytes--metabolism; Diet--adverse effects; Dietary Fats--adverse effects; Eating--immunology; Energy Metabolism--immunology; Gene Expression Regulation--immunology; Glucose Tolerance Test; Inflammation--genetics; Insulin--metabolism; Liver--immunology; Mice; Mice, Inbred BALB C; Natural Killer T-Cells--cytology; Natural Killer T-Cells--immunology; Obesity--etiology; Obesity--immunology; Obesity--metabolism; Obesity--physiopathology
Other ID: NLM PMC3108591
PubMed Central ID: PMC3108591
PubMed ID: 21674035
Date Deposited: 30 Aug 2012 14:30
Last Modified: 09 Jul 2019 16:55
URI: http://d-scholarship.pitt.edu/id/eprint/13864

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