The diagnosis and management of monogenic diabetes in children and adolescents

被引:141
作者
Hattersley, Andrew [1 ]
Bruining, Jan [2 ]
Shield, Julian [3 ]
Njolstad, Pal [4 ]
Donaghue, Kim C. [5 ]
机构
[1] Peninsula Med Sch, Inst Biomed & Clin Sci, Exeter EX2 5DW, Devon, England
[2] Sophia Childrens Univ Hosp, Rotterdam, Netherlands
[3] Univ Bristol, Dept Child Hlth, Bristol, Avon, England
[4] Univ Bergen, Dept Child Hlth, Bergen, Norway
[5] Univ Sydney, Childrens Hosp Westmead, Sydney, NSW 2006, Australia
关键词
HEPATOCYTE NUCLEAR FACTOR-1-ALPHA; WOLCOTT-RALLISON-SYNDROME; ACTIVATING MUTATIONS; MOLECULAR-GENETICS; OPTIC ATROPHY; MELLITUS; INSULIN; KIR6.2; GLUCOSE; SULFONYLUREAS;
D O I
10.1111/j.1399-5448.2009.00571.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
[No abstract available]
引用
收藏
页码:33 / 42
页数:10
相关论文
共 63 条
[51]   No deterioration in glycemic control in HNF-1 α maturity-onset diabetes of the young following transfer from long term insulin to sulphonylureas [J].
Shepherd, M ;
Pearson, ER ;
Houghton, J ;
Salt, G ;
Ellard, S ;
Hattersley, AT .
DIABETES CARE, 2003, 26 (11) :3191-3192
[52]   Mutations in the Kir6.2 subunit of the KATP channel and permanent neonatal diabetes:: New insights and new treatment [J].
Slingerland, AS ;
Hattersley, AT .
ANNALS OF MEDICINE, 2005, 37 (03) :186-195
[53]   Early-onset type-II diabetes mellitus (MODY4) linked to IPF1 [J].
Stoffers, DA ;
Ferrer, J ;
Clarke, WL ;
Habener, JF .
NATURE GENETICS, 1997, 17 (02) :138-139
[54]   Insulin gene mutations as a cause of permanent neonatal diabetes [J].
Stoy, Julie ;
Edghill, Emma L. ;
Flanagan, Sarah E. ;
Ye, Honggang ;
Paz, Veronica P. ;
Pluzhnikov, Anna ;
Below, Jennifer E. ;
Hayes, M. Geoffrey ;
Cox, Nancy J. ;
Lipkind, Gregory M. ;
Lipton, Rebecca B. ;
Greeley, Siri Atma W. ;
Patch, Ann-Marie ;
Ellard, Sian ;
Steiner, Donald F. ;
Hattersley, Andrew T. ;
Philipson, Louis H. ;
Bell, Graeme I. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (38) :15040-15044
[55]   Different genes, different diabetes: lessons from maturity-onset diabetes of the young [J].
Stride, A ;
Hattersley, AT .
ANNALS OF MEDICINE, 2002, 34 (03) :207-216
[56]   The genetic abnormality in the beta cell determines the response to an oral glucose load [J].
Stride, A ;
Vaxillaire, M ;
Tuomi, T ;
Barbetti, F ;
Njolstad, PR ;
Hansen, T ;
Costa, A ;
Conget, I ;
Pedersen, O ;
Sovik, O ;
Lorini, R ;
Groop, L ;
Froguel, P ;
Hattersley, AT .
DIABETOLOGIA, 2002, 45 (03) :427-435
[57]   Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD) caused by mutations in a novel gene (wolframin) coding for a predicted transmembrane protein [J].
Strom, TM ;
Hörtnagel, K ;
Hofmann, S ;
Gekeler, F ;
Scharfe, C ;
Rabl, W ;
Gerbitz, KD ;
Meitinger, T .
HUMAN MOLECULAR GENETICS, 1998, 7 (13) :2021-2028
[58]   Transient neonatal diabetes - Widening the understanding of the etiopathogenesis of diabetes [J].
Temple, IK ;
Gardner, RJ ;
Mackay, DJG ;
Barber, JCK ;
Robinson, DO ;
Shield, JPH .
DIABETES, 2000, 49 (08) :1359-1366
[59]   AGE-CORRECTED EMPIRICAL GENETIC RISK ESTIMATES FOR 1ST-DEGREE RELATIVES OF IDDM PATIENTS [J].
TILLIL, H ;
KOBBERLING, J .
DIABETES, 1987, 36 (01) :93-99
[60]   Improved prandial glucose control with lower risk of hypoglycemia with nateglinide than with glibenclamide in patients with maturity-onset diabetes of the young type 3 [J].
Tuomi, T ;
Sarelin, L ;
Honkanen, EH ;
Groop, LC ;
Isomaa, B .
DIABETES CARE, 2006, 29 (02) :189-194