Book chapter
The contribution of defects in insulin signaling in skeletal muscle to insulin resistance and type 2 diabetes
Advances in Structural Biology, pp.41-64
2000
DOI: 10.1016/S1064-6000(00)80004-6
Abstract
This chapter reviews the contribution of defects in insulin signaling in skeletal muscle to insulin resistance and type 2 diabetes. Glucose homeostasis is maintained in vivo through a balance among glucose disposal in multiple tissues, glucose production by hepatocytes, and absorption by the small intestine. In mammalian cells, glucose crosses cell membranes by facilitated diffusion mediated by a family of closely related glucose transport proteins (Gluts). Glucose transport into cells is essential for survival. Insulin enhances the disposal of glucose into certain tissues by binding its receptor on the cell surface and activating a series of reactions that leads ultimately to glucose uptake by a specific transporter, Glut4. There are several mechanisms for the perturbations in insulin signaling that are seen in insulin resistance. A normal activation by the insulin of its receptor in skeletal muscle results in the tyrosine phosphorylation of the cascades of signaling proteins. This leads to changes in gene expression, increases in the synthesis of glycogen, fat, and protein, and the activation of a number of enzymes involved principally in glucose regulation.
Details
- Title: Subtitle
- The contribution of defects in insulin signaling in skeletal muscle to insulin resistance and type 2 diabetes
- Creators
- Karen C McCowenE. Dale Abel
- Resource Type
- Book chapter
- Publication Details
- Advances in Structural Biology, pp.41-64
- DOI
- 10.1016/S1064-6000(00)80004-6
- ISSN
- 1064-6000
- Language
- English
- Date published
- 2000
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Biochemistry and Molecular Biology; Internal Medicine; Fraternal Order of Eagles Diabetes Research Center; Endocrinology and Metabolism
- Record Identifier
- 9984025298702771
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