Sensitivity to sulphonylureas in patients with hepatocyte nuclear factor-1α gene mutations: Evidence for pharmacogenetics in diabetes

Diabetic Medicine

Volumn 17, Issue 7, 2000, Pages 543-545

  Pearson, E R ^a   Liddell, W G ^a   Shepherd, M ^a   Corrall, R J ^b   Hattersley, A T ^a,c  

^a UNIVERSITY OF EXETER   (United Kingdom)

^b BRISTOL ROYAL INFIRMARY   (United Kingdom)

^c School of Postgraduate Medicine and Health Sciences   (United Kingdom)

Author keywords

Genetics; HNF 1 ; MODY; Pharmacogenetics; Sulphonylurea sensitivity

Indexed keywords

CHLORPROPAMIDE; FRUCTOSAMINE; GLIBENCLAMIDE; GLUCOSE; HEMOGLOBIN A1C; METFORMIN; NUCLEAR FACTOR I; SULFONYLUREA DERIVATIVE; TOLBUTAMIDE;

ADULT; ARTICLE; CASE REPORT; DRUG SENSITIVITY; FEMALE; GENE; GENE MUTATION; HUMAN; HYPOGLYCEMIA; MALE; MATURITY ONSET DIABETES MELLITUS; PHARMACOGENETICS;

ADULT; AMINO ACID SUBSTITUTION; CHLORPROPAMIDE; DIABETES MELLITUS, TYPE 2; DNA TRANSPOSABLE ELEMENTS; DNA-BINDING PROTEINS; FEMALE; GLYBURIDE; HEPATOCYTE NUCLEAR FACTOR 1; HEPATOCYTE NUCLEAR FACTOR 1-ALPHA; HEPATOCYTE NUCLEAR FACTOR 1-BETA; HUMANS; HYPOGLYCEMIC AGENTS; INSULIN; METFORMIN; MIDDLE AGED; NUCLEAR PROTEINS; POINT MUTATION; SULFONYLUREA COMPOUNDS; TRANSCRIPTION FACTORS;

EID: 0033847575     PISSN: 07423071     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1464-5491.2000.00305.x     Document Type: Article

References (9)

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4. A case of hepatocyte nuclear factor-1α diabetes/MODY3 masquerading as Type 1 diabetes in a Mexican-American adolescent and responsive to a low dose of sulfonylurea
5. Novel MODY3 mutations in the hepatocyte nuclear factor-1α gene. Evidence for a hyperexcitability of pancreatic β-cells to intravenous secretagogues in a glucose-tolerant carrier of a P447L mutation
6. Efficacy of metformin in the treatment of NIDDM
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8. Altered insulin secretory responses to glucose in diabetic and nondiabetic subjects with mutations in the diabetes susceptibility gene MODY3 on chromosome 12
9. Characterization of the MODY3 phenotype. Early-onset diabetes caused by an insulin secretion defect