Insulin regulates POMC neuronal plasticity to control glucose metabolism

Hypothalamic neurons respond to nutritional cues by altering gene expression and neuronal excitability. The mechanisms that control such adaptive processes remain unclear. Here we define populations of POMC neurons in mice that are activated or inhibited by insulin and thereby repress or inhibit hep...

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Published ineLife Vol. 7
Main Authors Dodd, Garron T, Michael, Natalie J, Lee-Young, Robert S, Mangiafico, Salvatore P, Pryor, Jack T, Munder, Astrid C, Simonds, Stephanie E, Brüning, Jens Claus, Zhang, Zhong-Yin, Cowley, Michael A, Andrikopoulos, Sofianos, Horvath, Tamas L, Spanswick, David, Tiganis, Tony
Format Journal Article
LanguageEnglish
Published England eLife Science Publications, Ltd 19.09.2018
eLife Sciences Publications Ltd
eLife Sciences Publications, Ltd
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Abstract Hypothalamic neurons respond to nutritional cues by altering gene expression and neuronal excitability. The mechanisms that control such adaptive processes remain unclear. Here we define populations of POMC neurons in mice that are activated or inhibited by insulin and thereby repress or inhibit hepatic glucose production (HGP). The proportion of POMC neurons activated by insulin was dependent on the regulation of insulin receptor signaling by the phosphatase TCPTP, which is increased by fasting, degraded after feeding and elevated in diet-induced obesity. TCPTP-deficiency enhanced insulin signaling and the proportion of POMC neurons activated by insulin to repress HGP. Elevated TCPTP in POMC neurons in obesity and/or after fasting repressed insulin signaling, the activation of POMC neurons by insulin and the insulin-induced and POMC-mediated repression of HGP. Our findings define a molecular mechanism for integrating POMC neural responses with feeding to control glucose metabolism.
AbstractList Hypothalamic neurons respond to nutritional cues by altering gene expression and neuronal excitability. The mechanisms that control such adaptive processes remain unclear. Here we define populations of POMC neurons in mice that are activated or inhibited by insulin and thereby repress or inhibit hepatic glucose production (HGP). The proportion of POMC neurons activated by insulin was dependent on the regulation of insulin receptor signaling by the phosphatase TCPTP, which is increased by fasting, degraded after feeding and elevated in diet-induced obesity. TCPTP-deficiency enhanced insulin signaling and the proportion of POMC neurons activated by insulin to repress HGP. Elevated TCPTP in POMC neurons in obesity and/or after fasting repressed insulin signaling, the activation of POMC neurons by insulin and the insulin-induced and POMC-mediated repression of HGP. Our findings define a molecular mechanism for integrating POMC neural responses with feeding to control glucose metabolism.
Audience Academic
Author Zhang, Zhong-Yin
Horvath, Tamas L
Tiganis, Tony
Mangiafico, Salvatore P
Brüning, Jens Claus
Simonds, Stephanie E
Munder, Astrid C
Andrikopoulos, Sofianos
Spanswick, David
Dodd, Garron T
Lee-Young, Robert S
Michael, Natalie J
Cowley, Michael A
Pryor, Jack T
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ContentType Journal Article
Copyright 2018, Dodd et al.
COPYRIGHT 2018 eLife Science Publications, Ltd.
2018, Dodd et al. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Keywords human biology
cellular signalling
mouse
insulin
neuroscience
protein tyrosine phosphatase
medicine
POMC neurons
glucose metabolism
hypothalamus
Language English
License 2018, Dodd et al.
This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
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SSID ssj0000748819
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Snippet Hypothalamic neurons respond to nutritional cues by altering gene expression and neuronal excitability. The mechanisms that control such adaptive processes...
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SubjectTerms Animals
Biochemistry
Brain
cellular signalling
Diabetes therapy
Excitability
Fasting
Feeding
Gene expression
Genes
Glucose
Glucose - metabolism
Human Biology and Medicine
Humans
Hypoglycemic Agents - administration & dosage
Hypoglycemic Agents - pharmacology
Hypothalamus
Hypothalamus - cytology
Insulin
Insulin - administration & dosage
Insulin - pharmacology
Insulin resistance
Kinases
Male
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Neuronal Plasticity - drug effects
Neuronal Plasticity - genetics
Neurons
Neurons - metabolism
Neuroscience
Nutrient deficiency
Obesity
Phosphatases
Physiological aspects
Plasticity (neural)
POMC neurons
Pro-Opiomelanocortin - genetics
Pro-Opiomelanocortin - metabolism
Proopiomelanocortin
protein tyrosine phosphatase
Protein Tyrosine Phosphatase, Non-Receptor Type 2 - genetics
Protein Tyrosine Phosphatase, Non-Receptor Type 2 - metabolism
Receptor, Insulin - genetics
Receptor, Insulin - metabolism
Rodents
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Title Insulin regulates POMC neuronal plasticity to control glucose metabolism
URI https://www.ncbi.nlm.nih.gov/pubmed/30230471
https://www.proquest.com/docview/2127572578
https://search.proquest.com/docview/2116128787
https://pubmed.ncbi.nlm.nih.gov/PMC6170188
https://doaj.org/article/fab6ed8d6e114ea6b2ada91531963160
Volume 7
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