Abstract
Peripheral administration of baclofen significantly reduced food intake and body weight increase in both diabetic (db/db) and diet-induced obese mice for 5 weeks, whereas it had no significant effects on energy balance in their lean control mice. Despite the decreased body weight, neuropeptide Y expression in the arcuate nucleus was significantly decreased, whereas pro-opiomelanocortin expression was significantly increased by baclofen treatment. These data demonstrate that the inhibitory effects of baclofen on body weight in the obese mice were mediated via the arcuate nucleus at least partially, and suggest that GABA(B) agonists could be a new therapeutic reagent for obesity.
MeSH terms
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Adipokines / blood
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Adipose Tissue, White / drug effects
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Adipose Tissue, White / pathology
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Administration, Oral
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Animals
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Anti-Obesity Agents / administration & dosage
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Anti-Obesity Agents / therapeutic use*
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Arcuate Nucleus of Hypothalamus / drug effects
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Arcuate Nucleus of Hypothalamus / metabolism
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Baclofen / administration & dosage
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Baclofen / therapeutic use*
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Blood Glucose / drug effects
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Diet
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Eating / drug effects*
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GABA Agonists / administration & dosage
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GABA Agonists / therapeutic use*
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GABA-B Receptor Agonists
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Male
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Mice
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Mice, Obese
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Neuropeptide Y / biosynthesis
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Neuropeptide Y / genetics
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Obesity / drug therapy*
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Obesity / metabolism
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Obesity / pathology
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Pro-Opiomelanocortin / biosynthesis
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Pro-Opiomelanocortin / genetics
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RNA, Messenger / metabolism
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Weight Loss*
Substances
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Adipokines
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Anti-Obesity Agents
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Blood Glucose
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GABA Agonists
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GABA-B Receptor Agonists
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Neuropeptide Y
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RNA, Messenger
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Pro-Opiomelanocortin
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Baclofen