Abstract
Insulin-resistance is a major problem associated with diabetes and that is increasing rapidly worldwide. Insulin is a peptide hormone secreted by the β-cells of the pancreatic islets of Langerhans in response to increased circulating levels of glucose and amino acids and it is essential for appropriate tissue development, growth, and maintenance of wholebody glucose homeostasis by regulating carbohydrate, lipid and protein metabolism. Insulin resistance is a defect in signal transduction. The signaling mechanisms involved in the various biologic responses to insulin remain somewhat elusive. This review focuses on the structure and activity of insulin receptor, inheritance of insulin resistance, insulin receptor and alleles, enzyme activity in insulin resistance, insulin receptor in phosphorylation and relating substrate. We have discussed insulin receptor substrate-family (IRS) related to insulin resistance, detail downstream signaling effects, GLUT4 vesicle translocation and related events, cytokine-mediated insulin resistance, and feedback control mechanisms. This review also focuses on insulin resistance in obesity-linked metabolic syndrome, insulin resistance related to plasma membrane disturbances and insulin resistance for exercise and cellular integrity. Finally, we can conclude that insulin resistance is really a complex phenomenon in which several genetic defects combine with environmental stresses.
Keywords: Insulin resistance, insulin receptor, signaling events, metabolic syndrome, genetic defects
Current Protein & Peptide Science
Title: Biochemical and Molecular Basis of Insulin Resistance
Volume: 7 Issue: 2
Author(s): Chiranjib Chakraborty
Affiliation:
Keywords: Insulin resistance, insulin receptor, signaling events, metabolic syndrome, genetic defects
Abstract: Insulin-resistance is a major problem associated with diabetes and that is increasing rapidly worldwide. Insulin is a peptide hormone secreted by the β-cells of the pancreatic islets of Langerhans in response to increased circulating levels of glucose and amino acids and it is essential for appropriate tissue development, growth, and maintenance of wholebody glucose homeostasis by regulating carbohydrate, lipid and protein metabolism. Insulin resistance is a defect in signal transduction. The signaling mechanisms involved in the various biologic responses to insulin remain somewhat elusive. This review focuses on the structure and activity of insulin receptor, inheritance of insulin resistance, insulin receptor and alleles, enzyme activity in insulin resistance, insulin receptor in phosphorylation and relating substrate. We have discussed insulin receptor substrate-family (IRS) related to insulin resistance, detail downstream signaling effects, GLUT4 vesicle translocation and related events, cytokine-mediated insulin resistance, and feedback control mechanisms. This review also focuses on insulin resistance in obesity-linked metabolic syndrome, insulin resistance related to plasma membrane disturbances and insulin resistance for exercise and cellular integrity. Finally, we can conclude that insulin resistance is really a complex phenomenon in which several genetic defects combine with environmental stresses.
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Cite this article as:
Chakraborty Chiranjib, Biochemical and Molecular Basis of Insulin Resistance, Current Protein & Peptide Science 2006; 7 (2) . https://dx.doi.org/10.2174/138920306776359759
| DOI https://dx.doi.org/10.2174/138920306776359759 |
Print ISSN 1389-2037 |
| Publisher Name Bentham Science Publisher |
Online ISSN 1875-5550 |
Call for Papers in Thematic Issues
Peptide and Peptidomimetics: Structure, Assembly, and Applications
Peptides are fundamental biomolecules, imparting structural support, biochemical regulation, and potent pharmacological activity. The therapeutic significance of peptides and peptidomimetics was first demonstrated by the discovery of Insulin, leading to the development of clinically important agents such as Captopril, Semaglutide, and Goserelin, and the antibiotic Lariocidin. Progress in peptide chemistry ...read more
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