The DOI matches its Crossref record; 88 of the 88 references it cites were found in a registry or an index.
Recognition and Management of Individuals With Hyperglycemia Because of a Heterozygous Glucokinase Mutation
Abstract
Glucokinase–maturity-onset diabetes of the young (GCK-MODY), also known as MODY2, is caused by heterozygous inactivating mutations in the GCK gene. GCK gene mutations are present in ∼1 in 1,000 of the population, but most are not diagnosed. They are common causes of MODY (10–60%): persistent incidental childhood hyperglycemia (10–60%) and gestational diabetes mellitus (1–2%). GCK-MODY has a unique pathophysiology and clinical characteristics, so it is best considered as a discrete genetic subgroup. People with GCK-MODY have a defect in glucose sensing; hence, glucose homeostasis is maintained at a higher set point resulting in mild, asymptomatic fasting hyperglycemia (5.4–8.3 mmol/L, HbA1c range 5.8–7.6% [40–60 mmol/mol]), which is present from birth and shows slight deterioration with age. Even after 50 years of mild hyperglycemia, people with GCK-MODY do not develop significant microvascular complications, and the prevalence of macrovascular complications is probably similar to that in the general population. Treatment is not recommended outside pregnancy because glucose-lowering therapy is ineffective in people with GCK-MODY and there is a lack of long-term complications. In pregnancy, fetal growth is primarily determined by whether the fetus inherits the GCK gene mutation from their mother. Insulin treatment of the mother is only appropriate when increased fetal abdominal growth on scanning suggests the fetus is unaffected. The impact on outcome of maternal insulin treatment is limited owing to the difficulty in altering maternal glycemia in these patients. Making the diagnosis of GCK-MODY through genetic testing is essential to avoid unnecessary treatment and investigations, especially when patients are misdiagnosed with type 1 or type 2 diabetes.
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Cites
Hyperglycemia and adverse pregnancy outcomes
(2008) · New England Journal of Medicine · doi:10.1056/nejmoa0707943 · Cited by 5,563
Molecular mechanisms and clinical pathophysiology of maturity-onset diabetes of the young
Fajans, S. S., Bell, G. I., & Polonsky, K. S. (2001) · New England Journal of Medicine · doi:10.1056/nejmra002168 · Cited by 1,123
Froguel, P., Zouali, H., Vionnet, N., Velho, G., Vaxillaire, M., Sun, F., Lesage, S., Stoffel, M., Takeda, J., Passa, P., et al. (1993) · New England Journal of Medicine · doi:10.1056/nejm199303113281005 · Cited by 735
Maturity-onset diabetes of the young (MODY): how many cases are we missing?
Shields, B. M., Hicks, S., Shepherd, M. H., Colclough, K., Hattersley, A. T., & Ellard, S. (2010) · Diabetologia · doi:10.1007/s00125-010-1799-4 · Cited by 725
Self-citationFroguel, P., Vaxillaire, M., Sun, F., Velho, G., Zouali, H., Butel, M. O., Lesage, S., Vionnet, N., Clément, K., Fougerousse, F., et al. (1992) · Nature · doi:10.1038/356162a0 · Cited by 630
Genetic cause of hyperglycaemia and response to treatment in diabetes
Pearson, E. R., Starkey, B. J., Powell, R. J., Gribble, F. M., Clark, P. M., & Hattersley, A. T. (2003) · The Lancet · doi:10.1016/s0140-6736(03)14571-0 · Cited by 607
Self-citationMutations in the glucokinase gene of the fetus result in reduced birth weight
Hattersley, A. T., Beards, F., Ballantyne, E., Appleton, M., Harvey, R., & Ellard, S. (1998) · Nature Genetics · doi:10.1038/953 · Cited by 594
Self-citationClinical implications of a molecular genetic classification of monogenic β-cell diabetes
Murphy, R., Ellard, S., & Hattersley, A. T. (2008) · Nature Clinical Practice Endocrinology & Metabolism · doi:10.1038/ncpendmet0778 · Cited by 502
Self-citationBalsells, M., Garcia-Patterson, A., Sola, I., Roque, M., Gich, I., & Corcoy, R. (2015) · BMJ · doi:10.1136/bmj.h102 · Cited by 498
Osbak, K. K., Colclough, K., Saint-Martin, C., Beer, N. L., Bellanné-Chantelot, C., Ellard, S., & Gloyn, A. L. (2009) · Human Mutation · doi:10.1002/humu.21110 · Cited by 485
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A Clinical Update on Gestational Diabetes Mellitus
Sweeting, A., Wong, J., Murphy, H. R., & Ross, G. P. (2022) · Endocrine Reviews · doi:10.1210/endrev/bnac003 · Cited by 928
Hattersley, A. T., Greeley, S. A. W., Polak, M., Rubio-Cabezas, O., Njølstad, P. R., Mlynarski, W., Castano, L., Carlsson, A., Raile, K., Chi, D. V., et al. (2018) · Pediatric Diabetes · doi:10.1111/pedi.12772 · Cited by 319
Self-citationWright, C. F., West, B., Tuke, M., Jones, S. E., Patel, K., Laver, T. W., Beaumont, R. N., Tyrrell, J., Wood, A. R., Frayling, T. M., et al. (2019) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2018.12.015 · Cited by 212
Self-citationGreeley, S. A. W., Polak, M., Njølstad, P. R., Barbetti, F., Williams, R., Castano, L., Raile, K., Chi, D. V., Habeb, A., Hattersley, A. T., et al. (2022) · Pediatric Diabetes · doi:10.1111/pedi.13426 · Cited by 211
Self-citationTreatment options for MODY patients: a systematic review of literature
Delvecchio, M., Pastore, C., & Giordano, P. (2020) · Diabetes Therapy · doi:10.1007/s13300-020-00864-4 · Cited by 172
Metadata
- Authors
- Chakera, A. J., Steele, A. M., Gloyn, A. L., Shepherd, M. H., Shields, B., Ellard, S., & Hattersley, A. T.
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2015-06-11
- Volume
- 38
- Issue
- 7
- Pages
- 1383-1392
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- OpenAlex
- W1925102358
- Cited by
- 289
- References
- 88
- FWCI
- 16.36
- Type
- journal article
- Language
- en
- Open access
- closed
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