Insulin Mutation Screening in 1,044 Patients With Diabetes
Author:
Edghill Emma L.1, Flanagan Sarah E.1, Patch Ann-Marie1, Boustred Chris1, Parrish Andrew1, Shields Beverley1, Shepherd Maggie H.2, Hussain Khalid3, Kapoor Ritika R.3, Malecki Maciej4, MacDonald Michael J.5, Støy Julie6, Steiner Donald F.67, Philipson Louis H.6, Bell Graeme I.68, Hattersley Andrew T.1, Ellard Sian1,
Affiliation:
1. Institute of Biomedical and Clinical Science, Peninsula Medical School, Exeter, U.K 2. Institute of Health and Social Care, Peninsula Medical School, Exeter, U.K 3. Department of Endocrinology, Great Ormond Street Hospital for Children NHS Trust and the Institute of Child Health, University College London, London, U.K 4. Department of Metabolic Diseases, Jagiellonian University, Krakow, Poland 5. Department of Pediatrics, University of Wisconsin Medical School, Madison, Wisconsin 6. Department of Medicine, The University of Chicago, Chicago, Illinois 7. Department of Biochemistry and Molecular Biology, The University of Chicago, Chicago, Illinois 8. Department of Human Genetics, The University of Chicago, Chicago, Illinois
Abstract
OBJECTIVE— Insulin gene (INS) mutations have recently been described as a cause of permanent neonatal diabetes (PND). We aimed to determine the prevalence, genetics, and clinical phenotype of INS mutations in large cohorts of patients with neonatal diabetes and permanent diabetes diagnosed in infancy, childhood, or adulthood.
RESEARCH DESIGN AND METHODS— The INS gene was sequenced in 285 patients with diabetes diagnosed before 2 years of age, 296 probands with maturity-onset diabetes of the young (MODY), and 463 patients with young-onset type 2 diabetes (nonobese, diagnosed <45 years). None had a molecular genetic diagnosis of monogenic diabetes.
RESULTS— We identified heterozygous INS mutations in 33 of 141 probands diagnosed at <6 months, 2 of 86 between 6 and 12 months, and none of 58 between 12 and 24 months of age. Three known mutations (A24D, F48C, and R89C) account for 46% of cases. There were six novel mutations: H29D, L35P, G84R, C96S, S101C, and Y103C. INS mutation carriers were all insulin treated from diagnosis and were diagnosed later than ATP-sensitive K+ channel mutation carriers (11 vs. 8 weeks, P < 0.01). In 279 patients with PND, the frequency of KCNJ11, ABCC8, and INS gene mutations was 31, 10, and 12%, respectively. A heterozygous R6C mutation cosegregated with diabetes in a MODY family and is probably pathogenic, but the L68M substitution identified in a patient with young-onset type 2 diabetes may be a rare nonfunctional variant.
CONCLUSIONS— We conclude that INS mutations are the second most common cause of PND and a rare cause of MODY. Insulin gene mutation screening is recommended for all diabetic patients diagnosed before 1 year of age.
Publisher
American Diabetes Association
Subject
Endocrinology, Diabetes and Metabolism,Internal Medicine
Reference30 articles.
1. Iafusco D, Stazi MA, Cotichini R, Cotellessa M, Martinucci ME, Mazzella M, Cherubini V, Barbetti F, Martinetti M, Cerutti F, Prisco F: Permanent diabetes mellitus in the first year of life. Diabetologia 45:798–804,2002 2. Edghill EL, Dix RJ, Flanagan SE, Bingley PJ, Hattersley AT, Ellard S, Gillespie KM: HLA genotyping supports a nonautoimmune etiology in patients diagnosed with diabetes under the age of 6 months. Diabetes 55:1895–1898,2006 3. Stanik J, Gasperikova D, Paskova M, Barak L, Javorkova J, Jancova E, Ciljakova M, Hlava P, Michalek J, Flanagan SE, Pearson E, Hattersley AT, Ellard S, Klimes I: Prevalence of permanent neonatal diabetes in Slovakia and successful replacement of insulin with sulfonylurea therapy in KCNJ11 and ABCC8 mutation carriers. J Clin Endocrinol Metab 92:1276–1282,2007 4. Polak M, Shield J: Neonatal and very-early-onset diabetes mellitus. Semin Neonatol 9:59–65,2004 5. Gloyn AL, Pearson ER, Antcliff JF, Proks P, Bruining GJ, Slingerland AS, Howard N, Srinivasan S, Silva JM, Molnes J, Edghill EL, Frayling TM, Temple IK, Mackay D, Shield JP, Sumnik Z, van Rhijn A, Wales JK, Clark P, Gorman S, Aisenberg J, Ellard S, Njolstad PR, Ashcroft FM, Hattersley AT: Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med 350:1838–1849,2004
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