Source:http://linkedlifedata.com/resource/pubmed/id/12364457
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
|
pubmed:dateCreated |
2002-10-4
|
pubmed:abstractText |
In adults with impaired glucose tolerance (IGT) and obesity (OB), an elevated proinsulin (PI) is predictive of type 2 diabetes mellitus (DM) and precedes the diagnosis by 5-20 yr. In type 2 DM, the PI is disproportionately elevated, i.e. increased PI/insulin ratio (PI/I). Few studies have evaluated PI in children at risk for type 2 DM. In the face of the current epidemic, we evaluated the relationship of PI and PI/I to IGT, insulin resistance (IR) defined by homeostasis model of assessment (HOMA), degree of OB, and stage of puberty in 70 girls (mean age 10.8 yr; body mass index z-score 3.5; ethnicity 64% Hispanic, 19% white, 16% African-American, and 1% other). Family history of DM was reported in 83%, and acanthosis nigricans was present in 80%. Subjects underwent a 2-h oral glucose tolerance test with glucose, insulin, and PI determinations every 30 min. All had normal hemoglobin A1c and fasting glucose. Five had IGT. With higher HOMA-IR, PI increased (P < 0.05), yet the ratio of fasting PI/I was lower (P < 0.05). Girls with body mass index z-score greater than 4 (n = 29) had higher PI than nonobese girls (n = 19, P < 0.05), but PI/I ratios were not different. PI-0 was increased in late puberty (n = 29), compared with prepuberty (n = 26, P < 0.05), but PI/I ratios showed no statistical difference. We found PI increased with increasing IR and OB in girls. Overall, PI/I was not different, suggesting the elevated PI reflects increased beta-cell output proportional to the elevated insulin in these groups and not a defect in PI processing or secretion. In fact, the lower fasting PI/I of the highest HOMA-IR quartile vs. the lowest HOMA quartile indicates more efficient conversion of PI to I in the presence of increasing IR in these girls.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0021-972X
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
87
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
4673-7
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:12364457-Adolescent,
pubmed-meshheading:12364457-African Continental Ancestry Group,
pubmed-meshheading:12364457-Body Mass Index,
pubmed-meshheading:12364457-Child,
pubmed-meshheading:12364457-Child, Preschool,
pubmed-meshheading:12364457-Diabetes Mellitus, Type 2,
pubmed-meshheading:12364457-European Continental Ancestry Group,
pubmed-meshheading:12364457-Fasting,
pubmed-meshheading:12364457-Female,
pubmed-meshheading:12364457-Glucose Tolerance Test,
pubmed-meshheading:12364457-Hispanic Americans,
pubmed-meshheading:12364457-Homeostasis,
pubmed-meshheading:12364457-Humans,
pubmed-meshheading:12364457-Hyperinsulinism,
pubmed-meshheading:12364457-Insulin Resistance,
pubmed-meshheading:12364457-Islets of Langerhans,
pubmed-meshheading:12364457-Obesity,
pubmed-meshheading:12364457-Proinsulin,
pubmed-meshheading:12364457-Puberty,
pubmed-meshheading:12364457-Risk Factors
|
pubmed:year |
2002
|
pubmed:articleTitle |
Proinsulin in girls: relationship to obesity, hyperinsulinemia, and puberty.
|
pubmed:affiliation |
Department of Pediatrics, Division of Pediatric Endocrinology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA. d61@columbia.edu
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|