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PLoS One. 2012;7(12):e51898. doi: 10.1371/journal.pone.0051898. Epub 2012 Dec 14.

Duodenal lipid sensing activates vagal afferents to regulate non-shivering brown fat thermogenesis in rats.

Author information

1
Department of Medicine, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA.

Abstract

Previous evidence indicates that duodenal lipid sensing engages gut-brain neurocircuits to determine food intake and hepatic glucose production, but a potential role for gut-brain communication in the control of energy expenditure remains to be determined. Here, we tested the hypothesis that duodenal lipid sensing activates a gut-brain-brown adipose tissue neuraxis to regulate thermogenesis. We demonstrate that direct administration of lipids into the duodenum increases brown fat temperature. Co-infusion of the local anesthetic tetracaine with duodenal lipids abolished the lipid-induced increase in brown fat temperature. Systemic administration of the CCKA receptor antagonist devazepide blocked the ability of duodenal lipids to increase brown fat thermogenesis. Parenchymal administration of the N-methyl-d-aspartate receptor blocker MK-801 directly into the caudomedial nucleus of the solitary tract also abolished duodenal lipid-induced activation of brown fat thermogenesis. These findings establish that duodenal lipid sensing activates a gut-brain-brown fat axis to determine brown fat temperature, and thereby reveal a previously unappreciated pathway that regulates thermogenesis.

PMID:
23251649
PMCID:
PMC3522613
DOI:
10.1371/journal.pone.0051898
[Indexed for MEDLINE]
Free PMC Article

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