Evidence that Reduced Leptin Levels, but Not an Aberrant Sequence of Leptin or its Receptor, Contribute to the Obesity Syndrome in NON Mice

M. Igel; W. Becker; L. Herberg; H.-G. Joost

doi:10.1055/s-2007-979875

Hormone and Metabolic Research, Table of Contents

Horm Metab Res 1996; 28(12): 669-673
DOI: 10.1055/s-2007-979875

Originals Basic

Evidence that Reduced Leptin Levels, but Not an Aberrant Sequence of Leptin or its Receptor, Contribute to the Obesity Syndrome in NON Mice

M. Igel¹ , W. Becker¹ , L. Herberg² , H.-G. Joost¹

¹Institut für Pharmakologie und Toxikologie der RWTH Aachen, Aachen, Germany
²Diabetesforschungsinstitut Düsseldorf, Düsseldorf, Germany

Abstract

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Abstract

NON mice exhibit a polygenic syndrome of mild obesity which is less pronounced than that of the ob and db strains. Here, we have shown that the syndrome is accompanied by a rise in leptin mRNA levels in adipose tissue, corresponding with the increase in adipose tissue mass. Surprisingly, levels of the leptin protein in adipose tissue and serum were comparable to those of lean control animals (BL57/KsJ-+/+), and markedly lower than those in db/db-mice. The coding regions of the cDNA sequences of both leptin and the leptin receptor from NON mice were identical with those of the wild-type sequences. We suggested that low levels of leptin in adipose tissue and serum contribute to the obesity of NON mice.

Key words

Leptin - ob Gene - NON Mouse - Obesity - Leptin Receptor

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