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- Title
Altered insulin secretory responses to glucose in subjects with a mutation in the MODY1 gene on chromosome 20.
- Authors
Byrne, Maria M.; Sturis, Jeppe; Fajans, Stefan S.; Ortiz, F. Javier; Stoltz, Anjanette; Stoffel, Markus; Smith, Marla J.; Bell, Graeme I.; Halter, Jeffrey B.; Polonsky, Kenneth S.; Byrne, M M; Sturis, J; Fajans, S S; Ortiz, F J; Stoltz, A; Stoffel, M; Smith, M J; Bell, G I; Halter, J B; Polonsky, K S
- Abstract
This study was undertaken to test the hypothesis that the diabetes susceptibility gene on chromosome 20q12 responsible for maturity-onset diabetes of the young (MODY) in a large kindred, the RW family, results in characteristic alterations in the dose-response relationships between plasma glucose concentration and insulin secretion rate (ISR) that differentiate this form of MODY from MODY in subjects with glucokinase mutations. Ten marker-positive subjects and six matched nondiabetic marker-negative subjects from the RW family received graded intravenous glucose infusions on two occasions separated by a 42-h continuous intravenous glucose infusion designed to prime the beta-cell to secrete more insulin in response to glucose. ISR was derived by deconvolution of peripheral C-peptide levels. Basal glucose and insulin levels were similar in marker-negative and marker-positive groups (5.3 +/- 0.2 vs. 5.0 +/- 0.2 mmol/l, P > 0.2, and 86.1 +/- 3.9 vs. 63.7 +/- 12.1 pmol/l, P > 0.1, respectively). However, the marker-positive subjects had defective insulin secretory responses to an increase in plasma glucose concentrations. Thus, as the glucose concentration was raised above 7 mmol/l, the slope of the curve relating glucose and ISR was significantly blunted in the marker-positive subjects (13 +/- 4 vs. 68 +/- 8 pmol.min-1.mmol-1 x 1, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
- Publication
Diabetes, 1995, Vol 44, Issue 6, p699
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/diab.44.6.699