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Leptin Perfusion Affects Insulin Secretion but Not Insulin Receptors in Rats

Mackowiak, P.; Nogowski, L.; Fabis, M.; Nowak, K.W.
Archives of Physiology and Biochemistry , Volume 109 (1) Informa HealthcareJan 1, 2001

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Leptin Perfusion Affects Insulin Secretion but Not Insulin Receptors in Rats

Abstract

The aim of the study was to investigate acute leptin effects on insulin secretion and liver insulin binding in rats in vitro. In the in situ experiments leptin changed the pattern of insulin secretion from the pancreas but did not influence insulin binding in the liver. Perfusion of the pancreas with leptin (1, 10, and 100 nmol/l, respectively) at physiological and supraphysiological levels of glucose (6.66 and 25.0 mmol/l, respectively) did not evoke the inhibition of insulin output observed by the authors previously in the in vivo manners. On the contrary, leptin perfusion resulted in stimulation of insulin secretion. Simultaneously, liver perfusion with leptin for 30 min did not influence specific insulin binding. Analysis of Scatchard' plots indicated no changes in the number of high- and low-affinity insulin receptors and in their affinity to the hormone. Additionally, leptin did not influence general carbohydrate and lipid metabolism of the perfused liver. After the treatment with leptin, the output of glucose, free fatty acids and triglycerides to perfusate and the final contents of glycogen and triglycerides in liver were comparable to values obtained in control animals. The results indicate that some in vitro effects exerted by leptin differ from those observed in vivo.
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Title
Leptin Perfusion Affects Insulin Secretion but Not Insulin Receptors in Rats
Author(s)
Mackowiak, P.; Nogowski, L.; Fabis, M.; Nowak, K.W.
Journal
Archives of Physiology and Biochemistry , Volume 109 (1) Informa Healthcare – Jan 1, 2001
Publisher
Informa UK Ltd
Copyright
© 2001 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted
Subject
Research Article
ISSN
1381-3455
eISSN
1744-4160
D.O.I.
10.1076/apab.109.1.63.4286
Publisher site
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