Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading-Reference-Cited by-同舟云学术

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Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading

Published:2019-05-17 Issue:24 Volume:76 Page:4887-4904
ISSN:1420-682X
Container-title:Cellular and Molecular Life Sciences
language:en
Short-container-title:Cell. Mol. Life Sci.

Author:

Nisr Raid B.,Shah Dinesh S.,Ganley Ian G.,Hundal Harinder S.

Funder

Diabetes UK

Biotechnology and Biological Sciences Research Council

Medical Research Council UK

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology,Cellular and Molecular Neuroscience,Pharmacology,Molecular Biology,Molecular Medicine

Link

http://link.springer.com/content/pdf/10.1007/s00018-019-03148-8.pdf

Reference71 articles.

1. Feve B, Bastard JP (2009) The role of interleukins in insulin resistance and type 2 diabetes mellitus. Nat Rev Endocrinol 5:305–311

2. Funaki M (2009) Saturated fatty acids and insulin resistance. J Med Invest 56:88–92

3. Jove M et al (2005) Palmitate-induced interleukin 6 production is mediated by protein kinase C and nuclear-factor kappaB activation and leads to glucose transporter 4 down-regulation in skeletal muscle cells. Endocrinology 146:3087–3095

4. Weigert C et al (2004) Palmitate, but not unsaturated fatty acids, induces the expression of interleukin-6 in human myotubes through proteasome-dependent activation of nuclear factor-kappaB. J Biol Chem 279:23942–23952

5. Boden G (2006) Fatty acid-induced inflammation and insulin resistance in skeletal muscle and liver. Curr Diab Rep 6:177–181

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