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The sibutramine metabolite M2 improves muscle glucose uptake and reduces hepatic glucose output: preliminary dataDivision of Diabetes, Department of Medicine, The University of Texas Health Science Center at San Antonio, Texas 78229-3900, US
Faculty of Life Sciences, University College London, London, UK
RenaSci Consultancy Limited, BioCity, Nottingham, UK
School of Life and Health Sciences, Aston University, Birmingham, UK The satiety agent sibutramine acts in part through a primary amine metabolite, M2. To investigate whether M2 could affect glycaemia independently of satiety and weight loss, groups of normal mice received a single dose of M2 (1 or 10 mg/kg) and food was withheld. Compared with controls (who received vehicle only), M2 (10 mg/kg) decreased basal plasma glucose concentrations, with a maximal decrease of about 25% at 4-8 hours (p<0.05). Soleus muscles were isolated from the mice at intervals: insulin-mediated glucose uptake by the muscles from controls progressively decreased over 24 hours whereas uptake was maintained by muscles from M2-treat-ed mice. Hepatic gluconeogenesis was reduced about 40% by liver snips isolated from M2-treated mice after 24 hours (p<0.05). These preliminary results suggest that the M2 metabolite of sibutramine can reduce glycaemia, maintain insulin-mediated muscle glucose uptake and reduce hepatic gluconeogenesis independently of satiety and weight loss.
Key Words: sibutramine basal plasma glucose insulin-mediated glucose uptake hepatic gluconeogenesis mice
Diabetes and Vascular Disease Research, Vol. 3, No. 3,
186-188 (2006) This article has been cited by other articles:
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