Abstract：
:Nicotine is known to stimulate energy expenditure, although the precise mechanism is unclear. To clarify the involvement of corticotropin-releasing factor (CRF) in the mechanism by which nicotine increases energy expenditure, the effect of intraperitoneal injection of nicotine (0.1 or 0.5mg/kg) on the release of noradrenaline (NA), a stimulator of thermogenesis, in brown adipose tissue (BAT) important for energy expenditure was examined in rats. We also examined the effects of CRF receptor subtype antagonists on the nicotine-induced change in BAT NA release. Nicotine significantly increased BAT NA release at a dose of 0.5mg/kg, and the increase was completely blocked by antalarmin, a CRF type 1 receptor antagonist, but not by antisauvagine-30, a CRF type 2 receptor antagonist. These results suggest that nicotine increases energy expenditure by activating BAT function, and that CRF type 1 receptors are involved in the mechanism by which nicotine affects energy balance.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Mano-Otagiri A,Iwasaki-Sekino A,Ohata H,Arai K,Shibasaki Tdoi
10.1016/j.neulet.2009.03.054subject
Has Abstractpub_date
2009-05-08 00:00:00pages
26-9issue
1eissn
0304-3940issn
1872-7972pii
S0304-3940(09)00351-6journal_volume
455pub_type
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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