Abstract
The author discusses a new study reporting the birth weight of patients carrying a mutation in either of two closely related genes associated with maturity-onset diabetes of the young, testing the hypothesis that the primary defect caused by these genes results in decreased insulin secretion.
Publication types
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Research Support, Non-U.S. Gov't
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Comment
MeSH terms
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Adult
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Age of Onset
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Animals
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Birth Weight
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Congenital Hyperinsulinism / genetics
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Congenital Hyperinsulinism / physiopathology
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Diabetes Mellitus, Type 2 / blood
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Diabetes Mellitus, Type 2 / etiology*
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Diabetes Mellitus, Type 2 / genetics
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Diabetes Mellitus, Type 2 / physiopathology
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Embryonic Development / genetics
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Female
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Fetal Macrosomia / etiology
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Fetal Macrosomia / genetics
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Fetal Macrosomia / physiopathology
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Genotype
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Hepatocyte Nuclear Factor 1-alpha / genetics
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Hepatocyte Nuclear Factor 1-alpha / physiology
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Hepatocyte Nuclear Factor 4 / deficiency
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Hepatocyte Nuclear Factor 4 / genetics
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Hepatocyte Nuclear Factor 4 / physiology
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Humans
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Hyperinsulinism / complications
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Hyperinsulinism / congenital
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Hyperinsulinism / embryology
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Hyperinsulinism / physiopathology
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Hypoglycemia / congenital
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Infant, Newborn
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Insulin / deficiency
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Insulin / metabolism*
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Insulin Resistance
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Insulin Secretion
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Islets of Langerhans / embryology
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Islets of Langerhans / metabolism
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Mice
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Mice, Knockout
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Phenotype
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Pregnancy
Substances
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HNF1A protein, human
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HNF4A protein, human
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Hepatocyte Nuclear Factor 1-alpha
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Hepatocyte Nuclear Factor 4
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Hnf4a protein, mouse
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Insulin