The beta cell glucokinase promoter variant is an unlikely risk factor for diabetes mellitus
Lotfi, K. ; Sund, G. ; Lowe, R. ; Graham, J. ; Landin-Olsson, M. LU ; Kockum, I. ; Deeb, S. and Lernmark, Å LU
(1997)
In Diabetologia
40(8).
p.959-962
- Abstract
Glucokinase plays an important role in the regulation of insulin secretion and is therefore an attractive candidate gene for both insulin dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. A single G-A nucleotide polymorphism at the -30 position of the beta-cell specific promoter region of the glucokinase gene was previously associated with reduced beta-cell function. In the present study we analysed 268 consecutive newly diagnosed Swedish patients classified with either IDDM (n = 205), NIDDM (n = 31) or unclassifiable (n = 32) diabetes between the ages of 15 and 35 years along with a group of 158 age- and sex-matched control subjects. The beta-cell promoter region was amplified by the polymerase chain reaction and... (More)
Glucokinase plays an important role in the regulation of insulin secretion and is therefore an attractive candidate gene for both insulin dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. A single G-A nucleotide polymorphism at the -30 position of the beta-cell specific promoter region of the glucokinase gene was previously associated with reduced beta-cell function. In the present study we analysed 268 consecutive newly diagnosed Swedish patients classified with either IDDM (n = 205), NIDDM (n = 31) or unclassifiable (n = 32) diabetes between the ages of 15 and 35 years along with a group of 158 age- and sex-matched control subjects. The beta-cell promoter region was amplified by the polymerase chain reaction and the G-A variant identified by single strand conformational polymorphism. There was no significant difference in allele frequencies of G and A between any of the subject groups and likewise, no significant difference in the frequencies of the G/G, G/A, or A/A genotypes. Eight subjects were homozygous for the less common A allele, five had IDDM and three were control subjects. Our results suggest that the -30 beta-cell glucokinase promoter variant is not associated with IDDM.
(Less)
- author
- Lotfi, K.
; Sund, G.
; Lowe, R.
; Graham, J.
; Landin-Olsson, M.
LU
; Kockum, I.
; Deeb, S.
and Lernmark, Å
LU
- publishing date
- 1997-08-11
- type
- Contribution to journal
- publication status
- published
- keywords
- GAD65 antibodies, Glucokinase gene, IDDM, Islet cell antibodies, NIDDM, Polymerase chain reaction, Single strand conformational polymorphism
- in
- Diabetologia
- volume
- 40
- issue
- 8
- pages
- 959 - 962
- publisher
- Springer
- external identifiers
-
- pmid:9267992
- scopus:0030787367
- ISSN
- 0012-186X
- DOI
- 10.1007/s001250050774
- language
- English
- LU publication?
- no
- id
- 0c2b4a8e-9b95-4063-9d52-c6501c012131
- date added to LUP
- 2019-07-01 13:16:54
- date last changed
- 2024-03-13 08:16:30
@article{0c2b4a8e-9b95-4063-9d52-c6501c012131,
abstract = {{<p>Glucokinase plays an important role in the regulation of insulin secretion and is therefore an attractive candidate gene for both insulin dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. A single G-A nucleotide polymorphism at the -30 position of the beta-cell specific promoter region of the glucokinase gene was previously associated with reduced beta-cell function. In the present study we analysed 268 consecutive newly diagnosed Swedish patients classified with either IDDM (n = 205), NIDDM (n = 31) or unclassifiable (n = 32) diabetes between the ages of 15 and 35 years along with a group of 158 age- and sex-matched control subjects. The beta-cell promoter region was amplified by the polymerase chain reaction and the G-A variant identified by single strand conformational polymorphism. There was no significant difference in allele frequencies of G and A between any of the subject groups and likewise, no significant difference in the frequencies of the G/G, G/A, or A/A genotypes. Eight subjects were homozygous for the less common A allele, five had IDDM and three were control subjects. Our results suggest that the -30 beta-cell glucokinase promoter variant is not associated with IDDM.</p>}},
author = {{Lotfi, K. and Sund, G. and Lowe, R. and Graham, J. and Landin-Olsson, M. and Kockum, I. and Deeb, S. and Lernmark, Å}},
issn = {{0012-186X}},
keywords = {{GAD65 antibodies; Glucokinase gene; IDDM; Islet cell antibodies; NIDDM; Polymerase chain reaction; Single strand conformational polymorphism}},
language = {{eng}},
month = {{08}},
number = {{8}},
pages = {{959--962}},
publisher = {{Springer}},
series = {{Diabetologia}},
title = {{The beta cell glucokinase promoter variant is an unlikely risk factor for diabetes mellitus}},
url = {{http://dx.doi.org/10.1007/s001250050774}},
doi = {{10.1007/s001250050774}},
volume = {{40}},
year = {{1997}},
}