Genetic cause of hyperglycaemia and response to treatment in diabetes (Q28212185)

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Ewan Pearson

object named as

Ewan R Pearson

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Andrew Tym Hattersley

6

object named as

Andrew T Hattersley

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author name string

Bryan J Starkey

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Penny M Clark

Efficacy of metformin in the treatment of NIDDM. Meta-analysis

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language of work or name

English

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publication date

18 October 2003

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published in

The Lancet

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volume

362

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issue

9392

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page(s)

1275-81

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cites work

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Hyperexcitability to sulphonylurea in MODY3.

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A case of hepatocyte nuclear factor-1 alpha diabetes/MODY3 masquerading as type 1 diabetes in a Mexican-American adolescent and responsive to a low dose of sulfonylurea

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

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Novel MODY3 Mutations in the Hepatocyte Nuclear Factor-1 Gene: Evidence for a Hyperexcitability of Pancreatic -cells to Intravenous Secretagogues in a Glucose-Tolerant Carrier of a P447L Mutation

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Homeostasis model assessment: insulin resistance and ?-cell function from fasting plasma glucose and insulin concentrations in man

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Correct homeostasis model assessment (HOMA) evaluation uses the computer program

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Comparison of insulin sensitivity tests across a range of glucose tolerance from normal to diabetes

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The CONSORT statement: revised recommendations for improving the quality of reports of parallel-group randomized trials

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The revised CONSORT statement for reporting randomized trials: explanation and elaboration

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Fructosamine, hemoglobin A1c, and measures of diabetic control

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Quantification of the relationship between insulin sensitivity and beta-cell function in human subjects. Evidence for a hyperbolic function.

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Accurate assessment of beta-cell function: the hyperbolic correction

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Altered insulin secretory responses to glucose in diabetic and nondiabetic subjects with mutations in the diabetes susceptibility gene MODY3 on chromosome 12.

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Characterization of the MODY3 phenotype. Early-onset diabetes caused by an insulin secretion defect

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Defective insulin secretion in hepatocyte nuclear factor 1alpha-deficient mice

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Defective pancreatic beta-cell glycolytic signaling in hepatocyte nuclear factor-1alpha-deficient mice

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Dominant-negative suppression of HNF-1alpha function results in defective insulin gene transcription and impaired metabolism-secretion coupling in a pancreatic beta-cell line.

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Molecular targets of a human HNF1 alpha mutation responsible for pancreatic beta-cell dysfunction

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Loss of HNF-1alpha function in mice leads to abnormal expression of genes involved in pancreatic islet development and metabolism

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Decreased glibenclamide uptake in hepatocytes of hepatocyte nuclear factor-1alpha-deficient mice: a mechanism for hypersensitivity to sulfonylurea therapy in patients with maturity-onset diabetes of the young, type 3 (MODY3).

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Overexpression of dominant-negative mutant hepatocyte nuclear fctor-1 alpha in pancreatic beta-cells causes abnormal islet architecture with decreased expression of E-cadherin, reduced beta-cell proliferation, and diabetes.

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7 January 2021

Hepatocyte nuclear factor-1alpha modulates pancreatic beta-cell growth by regulating the expression of insulin-like growth factor-1 in INS-1 cells

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Dominant-negative suppression of HNF-1 alpha results in mitochondrial dysfunction, INS-1 cell apoptosis, and increased sensitivity to ceramide-, but not to high glucose-induced cell death.

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Insulin secretion and insulin sensitivity in diabetic subgroups: studies in the prediabetic and diabetic state

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10.1016/S0140-6736(03)14571-0

Identifiers

DOI

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

14575972

1 reference

Consolidated OpenCitations Corpus – April 2017