期刊
EXPERIMENTAL GERONTOLOGY
卷 85, 期 -, 页码 88-94出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2016.09.013
关键词
Inflammation; Sarcopenia; Signaling pathways; Interleukin-6; Bone; Growth
资金
- National Institute of Diabetes and Digestive and Kidney Diseases [R01-DK094244]
- Boston Family Endowment Funds of the University of Florida Foundation
Inflammation and zinc dyshomeostasis are two common hallmarks of aging. A major zinc transporter ZIP14 (slc39a14) is upregulated by proinflammatory stimuli, e.g. interleukin-6. We have evaluated the influence of age on the Zip14 KO phenotype using wild-type (WT) and Zip14 knockout (KO) mice. Aging produced a major increase in serum IL-6 concentrations that was dramatically augmented in the Zip14 KO mice. In keeping with enhanced serum IL-6 concentrations, aging produced tissue-specific increases in zinc concentration of skeletal muscle and white adipose tissue. Metabolic endotoxemia produced by Zip14 ablation is maintained in aged KO mice. Muscle non-heme iron (NHI) was increased in aged WT mice but not in aged Zip14 KO mice demonstrating NHI uptake by muscle is ZIP14-dependent and increases with age. NF-kappa B and STAT3 activation was greater in aged mice, but was tissue specific and inversely related to tissue zinc. Micro-CT analysis revealed that Zip14 KO mice had markedly reduced trabecular bone that was greatly amplified with aging. These results demonstrate that the inflammation-responsive zinc transporter ZIP14 has phenotypic effects that are amplified with aging. (C) 2016 Elsevier Inc. All rights reserved.
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