Abstract | OBJECTIVE:
Sugar consumption has increased markedly over the last few decades and parallels the dramatic increase in overweight and obesity. Data obtained from animal studies suggest that the intestinal serotonergic system and herein particularly the serotonin receptor 3 (5-HT3R) may be involved in sugar detection and short-term control of food intake. Using a mouse model, we tested the hypothesis that blocking 5-HT3R prevents the development of sugar-induced obesity. DESIGN: For 8 weeks, C57BL/J6 mice were offered either water containing 30% glucose or plain water in addition to normal chow. The effect of oral treatment with the 5-HT3R antagonist, tropisetron (0.2 mg kg(-1) body weight), on body weight and caloric intake was studied. RESULTS: CONCLUSION: Our results suggest that 5-HT3R is a new target for the modulation of hepatic glucose metabolism and for the prevention of obesity.
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Authors | S Weber, V Volynets, G Kanuri, I Bergheim, S C Bischoff |
Journal | International journal of obesity (2005)
(Int J Obes (Lond))
Vol. 33
Issue 12
Pg. 1339-47
(Dec 2009)
ISSN: 1476-5497 [Electronic] England |
PMID | 19823183
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Glucose Transport Proteins, Facilitative
- Indoles
- RNA, Messenger
- Serotonin Antagonists
- Tropisetron
- Glucose
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Topics |
- Animals
- Body Weight
(drug effects, physiology)
- Gastrointestinal Motility
(drug effects, physiology)
- Glucose
(metabolism)
- Glucose Transport Proteins, Facilitative
(metabolism)
- Indoles
(administration & dosage)
- Mice
- Mice, Inbred C57BL
- Obesity
(metabolism, prevention & control)
- RNA, Messenger
(metabolism)
- Serotonin Antagonists
(administration & dosage)
- Tropisetron
- Weight Gain
(drug effects, physiology)
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