Linked Life Data

15046742

Source:http://linkedlifedata.com/resource/pubmed/id/15046742

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-3-29
pubmed:abstractText
Genetics and diet interact to cause type 2 diabetes mellitus and obesity. PCK1 has been implicated as one of many genes associated with type 2 diabetes mellitus. The common assumption is that mutations in PCK1 lead to excessive glucose production through hepatic gluconeogenesis. However, there is an alternative explanation, wherein mutations at the PCK1 locus could selectively affect PCK1 expression in adipose tissue. The result would be changes in glyceroneogenesis that would affect the storage and release of fatty acids. Here, we present the novel hypothesis that a variety of phenotypes could arise from mutations of the various tissue-specific control elements of PCK1. We also suggest specific quantitative metabolic traits that would accompany mutations that selectively affect PCK1 expression in adipose tissue.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1043-2760
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
129-35
pubmed:dateRevised
2004-12-20
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Disregulated glyceroneogenesis: PCK1 as a candidate diabetes and obesity gene.
pubmed:affiliation
Department of Cell Biology and Biochemistry, Stop 6540, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. elmus.beale@ttuhsc.edu
pubmed:publicationType
Journal Article, Review