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Diet-induced obesity has a differential effect on adipose tissue and macrophage inflammatory responses of young and old mice

Authors

  • Dayong Wu,

    Corresponding author
    1. Nutritional Immunology Laboratory, JM USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA
    • Nutritional Immunology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA
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    • Dayong Wu and Simin Nikbin Meydani share senior authorship.

    • Tel.: 617-556-3368; Fax: +617-556-3224

  • Zhihong Ren,

    1. Nutritional Immunology Laboratory, JM USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA
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  • Munkyong Pae,

    1. Nutritional Immunology Laboratory, JM USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA
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  • Sung Nim Han,

    1. Nutritional Immunology Laboratory, JM USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA
    2. Department of Food and Nutrition, Seoul National University, Seoul, Korea
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  • Simin Nikbin Meydani

    1. Nutritional Immunology Laboratory, JM USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA
    Search for more papers by this author
    • Dayong Wu and Simin Nikbin Meydani share senior authorship.


  • Any opinions, findings, conclusion, or recommendations expressed in this publication are those of the authors and do not necessarily reflect the view of the U.S. Department of Agriculture.

Abstract

Obesity and aging are both associated with increased inflammation in adipose tissue. In this study, we investigated effect of diet-induced obesity on inflammatory status in young and old mice. Young (2 months) and old (19 months) C57BL/6 mice were fed a low-fat (10%, LF) or high-fat (60%, HF) diet for 4.5 months. Adipose tissue from old/LF mice expressed higher levels of IL-1β, IL-6, TNFα, and cyclooxygenase-2 mRNA compared with young/LF mice. HF diet upregulated expression of all these inflammatory markers in young mice to the levels seen in the aged. Adipocytes, but not stromal vascular cells, from old/LF mice produced more IL-6, TNFα, and prostaglandin (PG)E2 than those from young/LF mice. HF diet resulted in an increase of all these markers produced by adipocytes in young, but only TNFα in old mice. PGE2 produced by peritoneal macrophages (Mϕ's) was upregulated with aging, and HF diet induced more IL-6, TNFα, and PGE2 production in young but not in old mice. Thus, HF diet/obesity induces an inflammatory state in both visceral fat cells and peritoneal Mϕ's of young mice, but not so in old mice. Together, these results suggest that HF diet-induced obesity may speed up the aging process as characterized by inflammatory status. This study also indicates that animals have a differential response, depending on their ages, to HF diet-induced obesity and inflammation. This age-related difference in response to HF diet should be considered when using inflammation status as a marker in investigating adverse health impacts of HF diet and obesity. © 2013 BioFactors, 2013

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