Targeted disruption of the glucose transporter 4 selectively in muscle causes insulin resistance and glucose intolerance

By A. Zisman, O. Peroni, E. Dale Abel, M. Michael, F. Mauvais-Jarvis, Bradford B. Lowell, J. F. Wojtaszewski, M. Hirshman, A. Virkamaki, Laurie J. Goodyear and 2 more. Nature Medicine, 2000

762 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/b353d45064a7ab89c5810270baa7e1e5468143fc

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In Molecular Biology

1. K. Copps
2. B. Thorens
3. M. White
4. Marc Uldry
5. I. Wood
6. P. Trayhurn
7. Jongsoon Lee
8. Byung-Cheol Lee

In Physiology

1. K. Copps
2. I. Wood
3. P. Trayhurn
4. M. White
5. Marc Uldry
6. Byung-Cheol Lee
7. Jongsoon Lee

Citations in the corpus

• Insulin receptor signaling in normal and insulin-resistant states. (2014, background): “Hyperglycemia induced by decreased glucose transport in skeletal muscle impairs adipose and hepatic insulin action (Zisman et al. 2000; Kim et al. 2001b) and induces insulin resistance through several pathways, which are all believed to be linked to oxidative stress (Evans et al.”
• Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, neutral): “Ablation of GLUT4 specifically in skeletal muscle led to glucose intolerance and severe impairments in insulin-mediated glucose disposal into muscle in mice as young as 8 weeks of age (730).”
• Glucose transporters (GLUT and SGLT): expanded families of sugar transport proteins (2003, background): “These developments are summarised here.”
• The SLC2 (GLUT) Family of Membrane Transporters (2013, neutral): “…overexpression studies (Hansen et al., 2000; Marshall and Mueckler, 1994; Ren et al., 1995) and adipose and/or muscle specific knock-out of Slc2a4 genes in mice (Abel et al., 2001; Kotani et al., 2004; Zisman et al., 2000) confirm an important role for GLUT4 expression in both of these tissues.”
• Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2 (2012, background): “IKKβ and JNK—Impaired glucose uptake and/or insulin resistance within adipose tissue can contribute to the development of type 2 diabetes [164], likely by altering its secretion of adipokines, such as adiponectin or retinol-binding protein 4 (reviewed in [165]).”
• The SLC2 family of facilitated hexose and polyol transporters (2004, background): “Such mice show severe insulin resistance and glucose intolerance from an early age [78].”