Linked Life Data

12523500

Source:http://linkedlifedata.com/resource/pubmed/id/12523500

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-1-13
pubmed:abstractText
Pancreatic beta-cell dysfunction and insulin resistance are two interrelated defects in the pathophysiology of type 2 diabetes. Defects in peripheral insulin action precede the development of glucose intolerance, as the pancreas compensates for insulin resistance by increasing insulin production and secretion. This may be achieved by enhancing cellular secretory capacity or by increasing beta-cell mass. Over time, the pancreatic secretion of insulin becomes inadequate for the extent of insulin resistance, and the levels of fasting and postprandial glucose rise leading to the onset of frank hyperglycemia, which leads to reduction in beta-cell function and survival through a process referred to as glucose toxicity. There is increasing evidence that apoptosis is the main mode of pancreatic beta-cell death not only in type 1 but also in type 2 diabetes. Recently, studies in knockout mice, human and rat islets, and pancreatic beta-cell lines demonstrated that defective insulin signaling in beta-cells might play an important pathophysiological role by affecting both secretory function and cell survival. The purpose of this review is to present recent advances in understanding of the interrelationship between molecular mechanisms underlying defects in insulin secretion and beta-cell survival in type 2 diabetes caused by impaired activation of insulin signaling pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0785-3890
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
444-50
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:12523500-Animals, pubmed-meshheading:12523500-Apoptosis, pubmed-meshheading:12523500-Cell Survival, pubmed-meshheading:12523500-Diabetes Mellitus, Type 2, pubmed-meshheading:12523500-Disease Models, Animal, pubmed-meshheading:12523500-Humans, pubmed-meshheading:12523500-Hyperplasia, pubmed-meshheading:12523500-Insulin, pubmed-meshheading:12523500-Insulin Receptor Substrate Proteins, pubmed-meshheading:12523500-Insulin Resistance, pubmed-meshheading:12523500-Insulin-Like Growth Factor I, pubmed-meshheading:12523500-Islets of Langerhans, pubmed-meshheading:12523500-Mice, pubmed-meshheading:12523500-Mice, Knockout, pubmed-meshheading:12523500-Phosphoproteins, pubmed-meshheading:12523500-Polymorphism, Genetic, pubmed-meshheading:12523500-Receptor, Insulin, pubmed-meshheading:12523500-Signal Transduction
pubmed:year
2002
pubmed:articleTitle
Apoptosis in the beta cells: cause or consequence of insulin secretion defect in diabetes?
pubmed:affiliation
Department of Experimental and Clinical Medicine, University of Catanzaro-Magna Graecia, IT-88100 Catanzaro, Italy. sesti@unicz.it
pubmed:publicationType
Journal Article, Review