Journal
CELL METABOLISM
Volume 21, Issue 5, Pages 692-705Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2015.04.008
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Funding
- University of Iowa Department of Neurology
- Novo Nordisk Foundation Center for Basic Metabolic Research
- Danish Research Council
- Lundbeck Foundation
- American Diabetes Association [7-13-JF-49]
- NIH [F32DK102347, DK059637, DK020593]
- Edward Mallinckrodt Jr. Foundation Grant
- NNF Center for Basic Metabolic Research [Gillum Group] Funding Source: researchfish
- Novo Nordisk Fonden [NNF14OC0009525] Funding Source: researchfish
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Thermogenic brown and beige adipocytes convert chemical energy to heat by metabolizing glucose and lipids. Serotonin (5-HT) neurons in the CNS are essential for thermoregulation and accordingly may control metabolic activity of thermogenic fat. To test this, we generated mice in which the human diphtheria toxin receptor (DTR) was selectively expressed in central 5-HT neurons. Treatment with diphtheria toxin (DT) eliminated 5-HT neurons and caused loss of thermoregulation, brown adipose tissue (BAT) steatosis, and a >50% decrease in uncoupling protein 1 (Ucp1) expression in BAT and inguinal white adipose tissue (WAT). In parallel, blood glucose increased 3.5-fold, free fatty acids 13.4-fold, and tri-glycerides 6.5-fold. Similar BAT and beige fat defects occurred in Lmx1b(f/f) ePet1(Cre) mice in which 5-HT neurons fail to develop in utero. We conclude 5-HT neurons play a major role in regulating glucose and lipid homeostasis, in part through recruitment and metabolic activation of brown and beige adipocytes.
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