Linked Life Data

2874367

Source:http://linkedlifedata.com/resource/pubmed/id/2874367

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8503
pubmed:dateCreated
1986-9-17
pubmed:abstractText
Continuous infusion of glucose with model assessment was used to measure glucose tolerance, beta-cell function, and insulin sensitivity in 154 first-degree relatives of 55 patients with type-2 diabetes. The plasma glucose achieved at 1 h was normally distributed in normal control subjects, but 31 (20%) of relatives of type-2 diabetics had values above the normal distribution mean +2 SD. Insulin secretion, assessed from the first or second phase plasma-C-peptide responses, was significantly lower in the glucose-intolerant relatives than in normoglycaemic relatives of similar sex, age, and obesity. beta-cell function, estimated by means of model analysis, was severely impaired in the glucose-intolerant relatives but was not impaired in the normoglycaemic relatives (geometric mean 41% and 109% of normal beta-cell response, respectively). Reduced beta-cell function was found with all degrees of glucose intolerance, whereas only the more severely hyperglycaemic relatives had impaired insulin sensitivity. This suggests that the primary defect in familial type-2 diabetes is beta-cell dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0140-6736
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
360-4
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Beta-cell dysfunction, rather than insulin insensitivity, is the primary defect in familial type 2 diabetes.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't