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

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...

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Veröffentlicht in:Proceedings of the National Academy of Sciences - PNAS 2013-03, Vol.110 (11), p.4333-4338
Hauptverfasser: Sabra-Makke, Lina, Maritan, Micol, Planchais, Julien, Boutant, Marie, Pégorier, Jean-Paul, Even, Patrick C., Vasseur-Cognet, Mireille, Bossard, Pascale
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container_title Proceedings of the National Academy of Sciences - PNAS
container_volume 110
creator Sabra-Makke, Lina
Maritan, Micol
Planchais, Julien
Boutant, Marie
Pégorier, Jean-Paul
Even, Patrick C.
Vasseur-Cognet, Mireille
Bossard, Pascale
description 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.
doi_str_mv 10.1073/pnas.1219262110
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subjects Adipose tissue
Agricultural sciences
Animals
Autonomic Nervous System Diseases - etiology
Autonomic Nervous System Diseases - genetics
Autonomic Nervous System Diseases - metabolism
Autonomic Nervous System Diseases - pathology
Biological Sciences
Blood glucose
Brain
Chickens
COUP Transcription Factor II - biosynthesis
COUP Transcription Factor II - genetics
Food intake
Gene expression
Glucose
Glucose - genetics
Glucose - metabolism
Heterozygote
Homeostasis
Hypersensitivity
Hypoglycemia
Hypoglycemia - complications
Hypoglycemia - genetics
Hypoglycemia - metabolism
Hypoglycemia - pathology
Insulin
Insulin resistance
Life Sciences
Mice
Mice, Transgenic
Nerve Tissue Proteins - biosynthesis
Nerve Tissue Proteins - genetics
Neurons
Neurons - metabolism
Neurons - pathology
Organ Specificity - genetics
Phenotypes
Secretion
Steroidogenic Factor 1 - genetics
Steroidogenic Factor 1 - metabolism
Type 1 diabetes mellitus
Ventromedial Hypothalamic Nucleus - metabolism
Ventromedial Hypothalamic Nucleus - pathology
title Hypothalamic ventromedial COUP-TFII protects against hypoglycemia-associated autonomic failure
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