期刊
ENDOCRINOLOGY
卷 148, 期 4, 页码 1550-1560出版社
ENDOCRINE SOC
DOI: 10.1210/en.2006-1389
关键词
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资金
- NIDDK NIH HHS [DK62179, DK70332, DK58148] Funding Source: Medline
- NINDS NIH HHS [NS045231] Funding Source: Medline
- Wellcome Trust [068303] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK062179, R01DK058148, R01DK070332, R56DK058148] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS045231] Funding Source: NIH RePORTER
The central melanocortin 4 receptor (MC4R) plays a critical role in energy homeostasis, although little is known regarding its role in the regulation of adaptive thermogenesis of brown adipose tissue (BAT). Here we show using retrograde transsynaptic tracing with attenuated pseudorabies virus coupled with dual-label immunohistochemistry that specific subsets of MC4R-expressing neurons in multiple nuclei of the central nervous system known to regulate sympathetic outflow polysynaptically connect with interscapular BAT(IBAT). Furthermore, we show that MC4R(-/-) and agouti-related peptide-treated mice are defective in HFdiet-induced up-regulation of uncoupling protein 1 in IBAT. Additionally, MC4R(-/-) mice exposed to 4 C for 4 h exhibit a defect in up-regulation of uncoupling protein 1 levels in IBAT. Our results provide a neuroanatomic substrate for MC4R regulating sympathetically mediated IBAT thermogenesis and demonstrate that the MC4R is critically required for acute high-fat- and cold-induced IBAT thermogenesis.
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