Journal
CELL METABOLISM
Volume 5, Issue 1, Pages 21-33Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2006.12.002
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Funding
- NIA NIH HHS [AG022880, R01 AG022880] Funding Source: Medline
- NIDDK NIH HHS [R01 DK074386, DK060711, DK061619, R01 DK060711, R01 DK061619, R01 DK070039, R01 DK070723-03, R01 DK070723, DK070039, DK070723, DK074386] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK070039, R01DK074386, R01DK060711, R01DK061619, R01DK070723] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG022880] Funding Source: NIH RePORTER
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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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