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A Systems Biology Approach to Study Metabolic SyndromeThe Beta Cell in Metabolic Syndrome

A Systems Biology Approach to Study Metabolic Syndrome: The Beta Cell in Metabolic Syndrome [The pancreatic beta cell is equipped with a highly sophisticated machinery to precisely sense the metabolic status of the organism and secrete the exactly appropriate amount of insulin to maintain blood glucose levels in a very narrow range. When the Metabolic Syndrome develops, insulin resistance imposes an additional burden on the beta cell, which then hypersecretes insulin to meet the demand. In the majority of individuals, the beta cell can sustain this additional workload and maintain normoglycemia. In a subset of predisposed individuals however, this compensatory response eventually fails and diabetes develops. Once diabetes is established, beta-cell function continues to deteriorate over time. The molecular and cellular mechanisms underlying beta-cell failure are not fully understood, although several hypotheses have been proposed. Amongst these, glucolipotoxicity; defective mitochondrial metabolism and oxidative stress; inflammation; amyloid deposits, disruption of autophagic flux; endoplasmic reticulum stress; beta-cell dedifferentiation and exhaustion from chronic hypersecretion probably contribute to some extent, perhaps at various stages of the disease progression and differently between individuals. Thus, beta-cell failure is likely mediated by a number of interrelated and complex mechanisms, which is reflected in the inability of the current therapeutic options to significantly slow down disease progression. This provides a strong argument for early interventions aimed at preventing the functional demise of pancreatic beta cells in the Metabolic Syndrome.] http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png

A Systems Biology Approach to Study Metabolic SyndromeThe Beta Cell in Metabolic Syndrome

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References (155)

Publisher
Springer International Publishing
Copyright
© Springer International Publishing Switzerland 2014
ISBN
978-3-319-01007-6
Pages
85 –109
DOI
10.1007/978-3-319-01008-3_5
Publisher site
See Chapter on Publisher Site

Abstract

[The pancreatic beta cell is equipped with a highly sophisticated machinery to precisely sense the metabolic status of the organism and secrete the exactly appropriate amount of insulin to maintain blood glucose levels in a very narrow range. When the Metabolic Syndrome develops, insulin resistance imposes an additional burden on the beta cell, which then hypersecretes insulin to meet the demand. In the majority of individuals, the beta cell can sustain this additional workload and maintain normoglycemia. In a subset of predisposed individuals however, this compensatory response eventually fails and diabetes develops. Once diabetes is established, beta-cell function continues to deteriorate over time. The molecular and cellular mechanisms underlying beta-cell failure are not fully understood, although several hypotheses have been proposed. Amongst these, glucolipotoxicity; defective mitochondrial metabolism and oxidative stress; inflammation; amyloid deposits, disruption of autophagic flux; endoplasmic reticulum stress; beta-cell dedifferentiation and exhaustion from chronic hypersecretion probably contribute to some extent, perhaps at various stages of the disease progression and differently between individuals. Thus, beta-cell failure is likely mediated by a number of interrelated and complex mechanisms, which is reflected in the inability of the current therapeutic options to significantly slow down disease progression. This provides a strong argument for early interventions aimed at preventing the functional demise of pancreatic beta cells in the Metabolic Syndrome.]

Published: Sep 25, 2013

Keywords: Beta-cell; Glucolipotoxicity; Insulin; Islet; Metabolic syndrome

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