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Mechanisms of ketamine action on lipid metabolism in rats

Published online by Cambridge University Press:  19 April 2005

T. Saranteas
Affiliation:
University of Athens, Department of Pharmacology, Medical School, Athens, Greece General Hospital of Athens, Department of Anaesthesiology, ‘G Gennimatas’, Athens, Greece
N. Zotos
Affiliation:
University of Athens, Department of Pharmacology, Medical School, Athens, Greece
E. Lolis
Affiliation:
University of Athens, Department of Pharmacology, Medical School, Athens, Greece University of Athens, Department of Surgery, Aretaieion Hospital of Athens, Athens, Greece
J. Stranomiti
Affiliation:
General Hospital of Athens, Department of Anaesthesiology, ‘G Gennimatas’, Athens, Greece
C. Mourouzis
Affiliation:
University of Athens, Department of Pharmacology, Medical School, Athens, Greece
C. Chantzi
Affiliation:
General Hospital of Athens, Department of Anaesthesiology, ‘G Gennimatas’, Athens, Greece
C. Tesseromatis
Affiliation:
University of Athens, Department of Pharmacology, Medical School, Athens, Greece
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Abstract

Summary

Background and objective: This study was conducted to determine the effect of ketamine on metabolic homoeostasis and particularly in lipoprotein lipase (LPL) activity in adipose tissue.

Methods: Sixty male Wistar rats were divided into six groups of 10 each. Group A served as controls, while Groups B–F received, respectively, ketamine 60, 80, 100, 120 and 140 mg kg−1 intraperitoneally. The animals were sacrificed 20 min after the administration of ketamine. Insulin concentrations in plasma and total cholesterol, triglyceride, high-density lipoprotein (HDL) and free fatty acid (FFA) concentrations in serum were measured. LPL activity in adipose tissue and medium-chain acyl-CoA dehydrogenase (MCAD) content in muscle were determined.

Results: FFA concentrations in serum significantly increased from the second lowest dose of ketamine. Insulin concentrations in plasma did not exhibit any significant difference between groups. MCAD levels were 0.5-fold more in Group F than in Group A, while there were no significant differences between control group and Groups B–E. Furthermore, high concentrations (120 and 140 mg kg−1) of ketamine interfered with in metabolic homoeostasis by significantly reducing LPL activity, thus elevating triglyceride concentrations in serum without affecting cholesterol and HDL metabolism.

Conclusions: Ketamine induces various metabolic effects due to changes in adipose LPL activity and MCAD levels in muscles. These findings seem to be significant only at high doses.

Type
Original Article
Copyright
2005 European Society of Anaesthesiology

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