Linked Life Data

17490424

Source:http://linkedlifedata.com/resource/pubmed/id/17490424

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-5-25
pubmed:abstractText
Large randomized studies have established that early intensive glycaemic control reduces the risk of diabetic complications, both micro- and macrovascular. However, epidemiological and prospective data support a long-term influence of early metabolic control on clinical outcomes. This phenomenon has recently been defined as 'metabolic memory.' Potential mechanisms for propagating this 'memory' are the non-enzymatic glycation of cellular proteins and lipids, and an excess of cellular reactive oxygen and nitrogen species, in particular originated at the level of glycated-mitochondrial proteins, perhaps acting in concert with one another to maintain stress signalling. Furthermore, the emergence of this 'metabolic memory' suggests the need for very early aggressive treatment aiming to 'normalize' glycaemic control and the addition of agents which reduce cellular reactive species and glycation in order to minimize long-term diabetic complications.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0742-3071
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
582-6
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Hypothesis: the 'metabolic memory', the new challenge of diabetes.
pubmed:affiliation
Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK.
pubmed:publicationType
Journal Article, Review