Type 2 diabetes: hypoinsulinism, hyperinsulinism, or both?

PLoS Med. 2007 Apr;4(4):e148. doi: 10.1371/journal.pmed.0040148.

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

  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Adult
  • Age of Onset
  • Animals
  • Birth Weight
  • Congenital Hyperinsulinism / genetics
  • Congenital Hyperinsulinism / physiopathology
  • Diabetes Mellitus, Type 2 / blood
  • Diabetes Mellitus, Type 2 / etiology*
  • Diabetes Mellitus, Type 2 / genetics
  • Diabetes Mellitus, Type 2 / physiopathology
  • Embryonic Development / genetics
  • Female
  • Fetal Macrosomia / etiology
  • Fetal Macrosomia / genetics
  • Fetal Macrosomia / physiopathology
  • Genotype
  • Hepatocyte Nuclear Factor 1-alpha / genetics
  • Hepatocyte Nuclear Factor 1-alpha / physiology
  • Hepatocyte Nuclear Factor 4 / deficiency
  • Hepatocyte Nuclear Factor 4 / genetics
  • Hepatocyte Nuclear Factor 4 / physiology
  • Humans
  • Hyperinsulinism / complications
  • Hyperinsulinism / congenital
  • Hyperinsulinism / embryology
  • Hyperinsulinism / physiopathology
  • Hypoglycemia / congenital
  • Infant, Newborn
  • Insulin / deficiency
  • Insulin / metabolism*
  • Insulin Resistance
  • Insulin Secretion
  • Islets of Langerhans / embryology
  • Islets of Langerhans / metabolism
  • Mice
  • Mice, Knockout
  • Phenotype
  • Pregnancy

Substances

  • HNF1A protein, human
  • HNF4A protein, human
  • Hepatocyte Nuclear Factor 1-alpha
  • Hepatocyte Nuclear Factor 4
  • Hnf4a protein, mouse
  • Insulin