Hypothalamic ventromedial COUP-TFII protects against hypoglycemia-associated autonomic failure

Proc Natl Acad Sci U S A. 2013 Mar 12;110(11):4333-8. doi: 10.1073/pnas.1219262110. Epub 2013 Feb 25.

Abstract

The nuclear receptor Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) is an important coordinator of glucose homeostasis through its function in different organs such as the endocrine pancreas, adipose tissue, skeletal muscle, and liver. Recently we have demonstrated that COUP-TFII expression in the hypothalamus is restricted to a subpopulation of neurons expressing the steroidogenic factor 1 transcription factor, known to play a crucial role in glucose homeostasis. To understand the functional significance of COUP-TFII expression in the steroidogenic factor 1 neurons, we generated hypothalamic ventromedial nucleus-specific COUP-TFII KO mice using the cyclization recombination/locus of X-overP1 technology. The heterozygous mutant mice display insulin hypersensitivity and a leaner phenotype associated with increased energy expenditure and similar food intake. These mutant mice also present a defective counterregulation to hypoglycemia with altered glucagon secretion. Moreover, the mutant mice are more likely to develop hypoglycemia-associated autonomic failure in response to recurrent hypoglycemic or glucopenic events. Therefore, COUP-TFII expression levels in the ventromedial nucleus are keys in the ability to resist the onset of hypoglycemia-associated autonomic failure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autonomic Nervous System Diseases / etiology
  • Autonomic Nervous System Diseases / genetics
  • Autonomic Nervous System Diseases / metabolism
  • Autonomic Nervous System Diseases / pathology
  • COUP Transcription Factor II / biosynthesis*
  • COUP Transcription Factor II / genetics
  • Chickens
  • Glucose / genetics
  • Glucose / metabolism*
  • Heterozygote
  • Hypoglycemia / complications
  • Hypoglycemia / genetics
  • Hypoglycemia / metabolism*
  • Hypoglycemia / pathology
  • Mice
  • Mice, Transgenic
  • Nerve Tissue Proteins / biosynthesis*
  • Nerve Tissue Proteins / genetics
  • Neurons / metabolism*
  • Neurons / pathology
  • Organ Specificity / genetics
  • Steroidogenic Factor 1 / genetics
  • Steroidogenic Factor 1 / metabolism
  • Ventromedial Hypothalamic Nucleus / metabolism*
  • Ventromedial Hypothalamic Nucleus / pathology

Substances

  • COUP Transcription Factor II
  • Nerve Tissue Proteins
  • Steroidogenic Factor 1
  • steroidogenic factor 1, mouse
  • Glucose