A Central Thermogenic-like Mechanism in Feeding Regulation: An Interplay between Arcuate Nucleus T3 and UCP2

Anna Coppola; Zhong-Wu Liu; Zane Bruce Andrews; Eric Paradis; Marie-Claude Roy; Jeffrey M Friedman; Daniel Ricquier; Denis Richard; Tamas L Horvath; Xiao-Bing Gao; Sabrina Diano

doi:10.1016/j.cmet.2006.12.002

A Central Thermogenic-like Mechanism in Feeding Regulation: An Interplay between Arcuate Nucleus T3 and UCP2

Anna Coppola, Zhong-Wu Liu, Zane Bruce Andrews, Eric Paradis, Marie-Claude Roy, Jeffrey M Friedman, Daniel Ricquier, Denis Richard, Tamas L Horvath, Xiao-Bing Gao, Sabrina Diano

Research output: Contribution to journal › Article › Research › peer-review

209 Citations (Scopus)

Abstract

The active thyroid hormone, triiodothyronine (T3), regulates mitochondrial uncoupling protein activity and related thermogenesis in peripheral tissues. Type 2 deiodinase (DII), an enzyme that catalyzes active thyroid hormone production, and mitochondrial uncoupling protein 2 (UCP2) are also present in the hypothalamic arcuate nucleus, where their interaction and physiological significance have not been explored. Here, we report that DII-producing glial cells are in direct apposition to neurons coexpressing neuropeptide Y (NPY), agouti-related protein (AgRP), and UCP2. Fasting increased DII activity and local thyroid hormone production in the arcuate nucleus in parallel with increased GDP-regulated UCP2-dependent mitochondrial uncoupling. Fasting-induced T3-mediated UCP2 activation resulted in mitochondrial proliferation in NPY/AgRP neurons, an event that was critical for increased excitability of these orexigenic neurons and consequent rebound feeding following food deprivation. These results reveal a physiological role for a thyroid-hormone-regulated mitochondrial uncoupling in hypothalamic neuronal networks.

Original language	English
Pages (from-to)	21 - 33
Number of pages	13
Journal	Cell Metabolism
Volume	5
Issue number	1
DOIs	https://doi.org/10.1016/j.cmet.2006.12.002
Publication status	Published - 2007
Externally published	Yes

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Cite this

@article{e151aa0e238b4b27b73122173a40b02e,

title = "A Central Thermogenic-like Mechanism in Feeding Regulation: An Interplay between Arcuate Nucleus T3 and UCP2",

abstract = "The active thyroid hormone, triiodothyronine (T3), regulates mitochondrial uncoupling protein activity and related thermogenesis in peripheral tissues. Type 2 deiodinase (DII), an enzyme that catalyzes active thyroid hormone production, and mitochondrial uncoupling protein 2 (UCP2) are also present in the hypothalamic arcuate nucleus, where their interaction and physiological significance have not been explored. Here, we report that DII-producing glial cells are in direct apposition to neurons coexpressing neuropeptide Y (NPY), agouti-related protein (AgRP), and UCP2. Fasting increased DII activity and local thyroid hormone production in the arcuate nucleus in parallel with increased GDP-regulated UCP2-dependent mitochondrial uncoupling. Fasting-induced T3-mediated UCP2 activation resulted in mitochondrial proliferation in NPY/AgRP neurons, an event that was critical for increased excitability of these orexigenic neurons and consequent rebound feeding following food deprivation. These results reveal a physiological role for a thyroid-hormone-regulated mitochondrial uncoupling in hypothalamic neuronal networks.",

author = "Anna Coppola and Zhong-Wu Liu and Andrews, {Zane Bruce} and Eric Paradis and Marie-Claude Roy and Friedman, {Jeffrey M} and Daniel Ricquier and Denis Richard and Horvath, {Tamas L} and Xiao-Bing Gao and Sabrina Diano",

year = "2007",

doi = "10.1016/j.cmet.2006.12.002",

language = "English",

volume = "5",

pages = "21 -- 33",

journal = "Cell Metabolism",

issn = "1550-4131",

publisher = "Elsevier",

number = "1",

}

A Central Thermogenic-like Mechanism in Feeding Regulation: An Interplay between Arcuate Nucleus T3 and UCP2. / Coppola, Anna; Liu, Zhong-Wu; Andrews, Zane Bruce; Paradis, Eric; Roy, Marie-Claude; Friedman, Jeffrey M; Ricquier, Daniel; Richard, Denis; Horvath, Tamas L; Gao, Xiao-Bing; Diano, Sabrina.

In: Cell Metabolism, Vol. 5, No. 1, 2007, p. 21 - 33.

Research output: Contribution to journal › Article › Research › peer-review

TY - JOUR

T1 - A Central Thermogenic-like Mechanism in Feeding Regulation: An Interplay between Arcuate Nucleus T3 and UCP2

AU - Coppola, Anna

AU - Liu, Zhong-Wu

AU - Andrews, Zane Bruce

AU - Paradis, Eric

AU - Roy, Marie-Claude

AU - Friedman, Jeffrey M

AU - Ricquier, Daniel

AU - Richard, Denis

AU - Horvath, Tamas L

AU - Gao, Xiao-Bing

AU - Diano, Sabrina

PY - 2007

Y1 - 2007

N2 - The active thyroid hormone, triiodothyronine (T3), regulates mitochondrial uncoupling protein activity and related thermogenesis in peripheral tissues. Type 2 deiodinase (DII), an enzyme that catalyzes active thyroid hormone production, and mitochondrial uncoupling protein 2 (UCP2) are also present in the hypothalamic arcuate nucleus, where their interaction and physiological significance have not been explored. Here, we report that DII-producing glial cells are in direct apposition to neurons coexpressing neuropeptide Y (NPY), agouti-related protein (AgRP), and UCP2. Fasting increased DII activity and local thyroid hormone production in the arcuate nucleus in parallel with increased GDP-regulated UCP2-dependent mitochondrial uncoupling. Fasting-induced T3-mediated UCP2 activation resulted in mitochondrial proliferation in NPY/AgRP neurons, an event that was critical for increased excitability of these orexigenic neurons and consequent rebound feeding following food deprivation. These results reveal a physiological role for a thyroid-hormone-regulated mitochondrial uncoupling in hypothalamic neuronal networks.

AB - The active thyroid hormone, triiodothyronine (T3), regulates mitochondrial uncoupling protein activity and related thermogenesis in peripheral tissues. Type 2 deiodinase (DII), an enzyme that catalyzes active thyroid hormone production, and mitochondrial uncoupling protein 2 (UCP2) are also present in the hypothalamic arcuate nucleus, where their interaction and physiological significance have not been explored. Here, we report that DII-producing glial cells are in direct apposition to neurons coexpressing neuropeptide Y (NPY), agouti-related protein (AgRP), and UCP2. Fasting increased DII activity and local thyroid hormone production in the arcuate nucleus in parallel with increased GDP-regulated UCP2-dependent mitochondrial uncoupling. Fasting-induced T3-mediated UCP2 activation resulted in mitochondrial proliferation in NPY/AgRP neurons, an event that was critical for increased excitability of these orexigenic neurons and consequent rebound feeding following food deprivation. These results reveal a physiological role for a thyroid-hormone-regulated mitochondrial uncoupling in hypothalamic neuronal networks.

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DO - 10.1016/j.cmet.2006.12.002

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