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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2009-5-7
pubmed:abstractText
We investigated a possible role of the central glucagon-like peptide (GLP-1) receptor system as an essential brain circuit regulating adiposity through effects on nutrient partitioning and lipid metabolism independent from feeding behavior. Both lean and diet-induced obesity mice were used for our experiments. GLP-1 (7-36) amide was infused in the brain for 2 or 7 d. The expression of key enzymes involved in lipid metabolism was measured by real-time PCR or Western blot. To test the hypothesis that the sympathetic nervous system may be responsible for informing adipocytes about changes in CNS GLP-1 tone, we have performed direct recording of sympathetic nerve activity combined with experiments in genetically manipulated mice lacking beta-adrenergic receptors. Intracerebroventricular infusion of GLP-1 in mice directly and potently decreases lipid storage in white adipose tissue. These effects are independent from nutrient intake. Such CNS control of adipocyte metabolism was found to depend partially on a functional sympathetic nervous system. Furthermore, the effects of CNS GLP-1 on adipocyte metabolism were blunted in diet-induced obese mice. The CNS GLP-1 system decreases fat storage via direct modulation of adipocyte metabolism. This CNS GLP-1 control of adipocyte lipid metabolism appears to be mediated at least in part by the sympathetic nervous system and is independent of parallel changes in food intake and body weight. Importantly, the CNS GLP-1 system loses the capacity to modulate adipocyte metabolism in obese states, suggesting an obesity-induced adipocyte resistance to CNS GLP-1.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
6
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5916-25
pubmed:dateRevised
2009-10-21
pubmed:meshHeading
pubmed-meshheading:19420258-Adipose Tissue, pubmed-meshheading:19420258-Analysis of Variance, pubmed-meshheading:19420258-Animals, pubmed-meshheading:19420258-Body Composition, pubmed-meshheading:19420258-Central Nervous System, pubmed-meshheading:19420258-Eating, pubmed-meshheading:19420258-Energy Metabolism, pubmed-meshheading:19420258-Glucagon-Like Peptide 1, pubmed-meshheading:19420258-Lipid Metabolism, pubmed-meshheading:19420258-Male, pubmed-meshheading:19420258-Mice, pubmed-meshheading:19420258-Mice, Inbred C57BL, pubmed-meshheading:19420258-Mice, Knockout, pubmed-meshheading:19420258-Motor Activity, pubmed-meshheading:19420258-Obesity, pubmed-meshheading:19420258-Peptide Fragments, pubmed-meshheading:19420258-Receptors, Adrenergic, beta, pubmed-meshheading:19420258-Receptors, Glucagon, pubmed-meshheading:19420258-Signal Transduction, pubmed-meshheading:19420258-Sympathetic Nervous System, pubmed-meshheading:19420258-Time Factors
pubmed:year
2009
pubmed:articleTitle
Direct control of peripheral lipid deposition by CNS GLP-1 receptor signaling is mediated by the sympathetic nervous system and blunted in diet-induced obesity.
pubmed:affiliation
Department of Psychiatry, Obesity Research Centre, University of Cincinnati, Cincinnati, Ohio 45226, USA. ruben.nogueiras@usc.es
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't