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Systemic CCK increases brown adipose tissue sympathetic nerve activity
Author(s) -
Madden Christopher J
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1120.5
Subject(s) - brown adipose tissue , endocrinology , adipose tissue , thermogenesis , medicine , vagus nerve , chloralose , cholecystokinin , vagotomy , sympathetic nervous system , thermoregulation , chemistry , biology , stimulation , blood pressure , receptor
The neural circuits responsible for governing sympathetic outflow to brown adipose tissue in response to thermoregulatory and febrile stimuli are very well characterized. In contrast we are only beginning to understand the organization of the metabolic regulation of the sympathetic outflow to brown adipose. The current study determines whether cholecystokine (CCK), a gut hormone released postprandially, activates brown adipose tissue sympathetic nerve activity via the vagus nerve. In urethane/chloralose anesthetized rats (n=3), intravenous administration of cholecystokinin (CCK, 0.5μg/kg) increased brown adipose tissue sympathetic nerve activity (BAT SNA: +141 ± 39% control), brown adipose tissue temperature (+0.5 ± 0.1 oC) and expired CO2 (+0.5 ± 0.1%). The CCK‐evoked increases in BAT SNA, BAT temperature and expired CO2 were sustained for at least 40 minutes. Bilateral cervical vagotomy prevented the CCK‐evoked increases in BAT SNA, BAT temperature and expired CO2 (n=2). These results indicate that peripheral CCK acts via vagal afferents to increase metabolism, energy expenditure and thermogenesis in BAT. The neural circuitry mediating this effect and the physiological significance of this system are under investigation.