The sibutramine metabolite M2 improves muscle glucose uptake and reduces hepatic glucose output: Preliminary data

Dawn K. Coletta, Sarah H. Bates, Robert B. Jones, Clifford J. Bailey

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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-treated 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.

Original languageEnglish (US)
Pages (from-to)186-188
Number of pages3
JournalDiabetes and Vascular Disease Research
Volume3
Issue number3
DOIs
StatePublished - Dec 1 2006
Externally publishedYes

Fingerprint

sibutramine
Glucose
Muscles
Gluconeogenesis
Liver
Weight Loss
Insulin
Amines
Skeletal Muscle
Food

Keywords

  • Basal plasma glucose
  • Hepatic gluconeogenesis
  • Insulin-mediated glucose uptake
  • Mice
  • Sibutramine

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Cardiology and Cardiovascular Medicine

Cite this

The sibutramine metabolite M2 improves muscle glucose uptake and reduces hepatic glucose output : Preliminary data. / Coletta, Dawn K.; Bates, Sarah H.; Jones, Robert B.; Bailey, Clifford J.

In: Diabetes and Vascular Disease Research, Vol. 3, No. 3, 01.12.2006, p. 186-188.

Research output: Contribution to journalArticle

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