Sökning: WFRF:(Njolstad I)
> (2002-2004) >
The genetic abnorma...
The genetic abnormality in the beta cell determines the response to an oral glucose load
-
Stride, A (författare)
-
Vaxillaire, M (författare)
-
Tuomi, T (författare)
-
visa fler...
-
Barbetti, F (författare)
-
Njolstad, PR (författare)
-
Hansen, T (författare)
-
Costa, A (författare)
-
Conget, I (författare)
-
Pedersen, O (författare)
-
Sovik, O (författare)
-
Lorini, R (författare)
-
- Groop, Leif (författare)
- Lund University,Lunds universitet,Genomik, diabetes och endokrinologi,Forskargrupper vid Lunds universitet,Genomics, Diabetes and Endocrinology,Lund University Research Groups
-
Froguel, P (författare)
-
Hattersley, AT (författare)
-
visa färre...
-
(creator_code:org_t)
- 2014-04-05
- 2002
- Engelska.
-
Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 45:3, s. 427-435
- Relaterad länk:
-
http://dx.doi.org/10...
-
visa fler...
-
https://link.springe...
-
https://lup.lub.lu.s...
-
https://doi.org/10.1...
-
visa färre...
Abstract
Ämnesord
Stäng
- Aims/hypothesis. We assessed how the role of genes genetic causation in causing maturity-onset diabetes of the young (MODY) alters the response to an oral glucose tolerance test (OGTT). Methods. We studied OGTT in 362 MODY subjects, from seven European centres; 245 had glucokinase gene mutations and 117 had Hepatocyte Nuclear Factor-1 alpha (HNF-1alpha) gene mutations. Results. BMI and age were similar in the genetically defined groups. Fasting plasma glucose (FPG) was less than 5.5 mmol/l in 2% glucokinase subjects and 46% HNF-1alpha subjects (p < 0.0001). Glucokinase subjects had a higher FPG than HNF-1a subjects ([means +/- SD] 6.8 +/- 0.8 vs 6.0 +/- 1.9 mmol/l, p < 0.0001), a lower 2-h value (8.9 +/- 2.3 vs 11.2 +/- 5.2 mmol/l, p < 0.0001) and a lower OGTT increment (2-h - fasting) (2.1 +/- 2.3 vs 5.2 +/- 3.9 mmol/l, p < 0.0001). The relative proportions classified as diabetic depended on whether fasting (38% vs 22%, glucokinase vs HNF-1alpha) or 2-h values (19% vs 44%) were used. Fasting and 2-h glucose values were not correlated in the glucokinase subjects (r = -0.047, p = 0.65) but were strongly correlated in HNF-1alpha subjects (r = 0.8, p < 0.001). Insulin concentrations were higher in the glucokinase subjects throughout the OGTT. Conclusion/interpretation. The genetic cause of the beta-cell defect results in clear differences in both the fasting glucose and the response to an oral glucose load and this can help diagnostic genetic testing in MODY. OGTT results reflect not only the degree of hyperglycaemia but also the underlying cause.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)
Nyckelord
- oral glucose tolerance test
- glucokinase
- alpha
- hepatocyte nuclear factor-1
- maturity-onset diabetes of the young
- MODY
- genetics
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
Hitta via bibliotek
Till lärosätets databas
- Av författaren/redakt...
-
Stride, A
-
Vaxillaire, M
-
Tuomi, T
-
Barbetti, F
-
Njolstad, PR
-
Hansen, T
-
visa fler...
-
Costa, A
-
Conget, I
-
Pedersen, O
-
Sovik, O
-
Lorini, R
-
Groop, Leif
-
Froguel, P
-
Hattersley, AT
-
visa färre...
- Om ämnet
-
- MEDICIN OCH HÄLSOVETENSKAP
-
MEDICIN OCH HÄLS ...
-
och Klinisk medicin
-
och Endokrinologi oc ...
- Artiklar i publikationen
-
Diabetologia
- Av lärosätet
-
Lunds universitet