Linked Life Data

19490821

Source:http://linkedlifedata.com/resource/pubmed/id/19490821

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-6-3
pubmed:abstractText
Early interventions to prevent type 2 diabetes mellitus (T2DM) demand a better understanding of its underlying mechanisms. Nonobese healthy subjects with a strong family history of T2DM (FH(+) subjects) hold a key to this end by allowing the study of the disease before the development of confounding factors, such as obesity or hyperglycemia. In this article, we share our experience over the past decade in studying FH(+) subjects and how lipotoxicity alters glucose metabolism in such individuals, in particular pancreatic beta-cell function. FH(+) subjects have no obvious clinical abnormalities, but when carefully studied, reveal severe hepatic/muscle/adipose tissue insulin resistance and subtle defects in beta-cell function. In most subjects, metabolic adaption allows freedom from diabetes for decades. However, the obesity epidemic is drastically changing this. Given the unique susceptibility of pancreatic beta cells to free fatty acids in FH(+) subjects, interventions that protect against obesity-induced lipotoxicity may hold the greatest promise for preventing T2DM in genetically predisposed individuals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1539-0829
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
200-7
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Lessons learned from studying families genetically predisposed to type 2 diabetes mellitus.
pubmed:affiliation
Diabetes Division, Department of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. cusi@uthscsa.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't