Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation.

By P. Plomgaard, K. Bouzakri, R. Krogh-Madsen, B. Mittendorfer, J. Zierath, B. K. Pedersen. Diabetes, 2005

635 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/51e4cf3e7fd0760935554ca26738f902ac429f30

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Patrice D Cani
2. G. Steinberg
3. Bruce E. Kemp
4. B. K. Pedersen
5. M. Febbraio
6. M. Quon
7. A. Neyrinck
8. Haiming Cao

In Molecular Biology

1. Patrice D Cani
2. B. K. Pedersen
3. K. Copps
4. A. Neyrinck
5. G. Steinberg
6. J. Hawley
7. M. White
8. R. Burcelin

In Physiology

1. B. K. Pedersen
2. G. Steinberg
3. Bruce E. Kemp
4. M. Febbraio
5. K. Copps
6. Patrice D Cani
7. A. Neyrinck
8. J. Hawley

Citations in the corpus

• Interleukin-6 Increases Insulin-Stimulated Glucose Disposal in Humans and Glucose Uptake and Fatty Acid Oxidation In Vitro via AMP-Activated Protein Kinase (2006, background): “menced and was maintained for 4 h (19).”
• Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia (2007, background): “Cytokines have been shown to cause insulin resistance [5, 6], which favours hyperinsulinaemia and excessive hepatic and adipose tissue lipid storage.”
• Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2 (2012, background): “TNFα activates multiple kinases in muscle, including S6K, ERK1/2, IKKβ and the IRS1 mS307/hS312 kinase JNK1; however, muscle hS312 phosphorylation is not significantly elevated by TNFα infusion prior to the period in which TNFα causes reduced IRS1 tyrosine phosphorylation and insulin resistance [34]”
• The Molecular Bases of Training Adaptation (2007, background): “Elevated TNFα concentration generates an increase in the activity of ubiquitin-conjugated protein degradation and inhibition of insulin / IGF mediated protein synthesis (GarciaMartinez et al. 1993; Garcia-Martinez et al. 1994; Fernandez-Celemin et al. 2002; Plomgaard et al. 2005; Williamson et al. 2”
• Cardiovascular actions of insulin. (2007, background): “Similarly, systemic infusion of TNF- to achieve circulating concentrations slightly higher than those observed in chronic inflammation such as diabetes reduced glucose disposal in healthy individuals (296).”