A human leptin mutant induces weight gain in normal mice
Leptin, a fat secreted hormone, regulates ingestive behaviour and energy balance by binding to a specific receptor. Using site-directed mutagenesis, we screened for single amino acid residues in human leptin which are critical for receptor binding and biological activity. Here we report that one of...
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| Published in | FEBS letters Vol. 405; no. 2; pp. 237 - 240 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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England
Elsevier B.V
24.03.1997
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| Abstract | Leptin, a fat secreted hormone, regulates ingestive behaviour and energy balance by binding to a specific receptor. Using site-directed mutagenesis, we screened for single amino acid residues in human leptin which are critical for receptor binding and biological activity. Here we report that one of these mutants has in vivo antagonistic properties. An Arg to Gln substitution at position 128 of human leptin does not affect receptor binding but knocks out biological activity. Repeated injection of R128Q in normal C57BL/6J mice results in a progressive increase in body weight. This demonstrates that R128Q is able to interfere with the negative feedback control of endogenous leptin. This mutant could be of therapeutic use for wasting disorders, such as anorexia and cachexia, where weight gain would be beneficial.
©1997 Federation of European Biochemical Societies. |
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| AbstractList | Leptin, a fat secreted hormone, regulates ingestive behaviour and energy balance by binding to a specific receptor. Using site-directed mutagenesis, we screened for single amino acid residues in human leptin which are critical for receptor binding and biological activity. Here we report that one of these mutants has in vivo antagonistic properties. An Arg to Gln substitution at position 128 of human leptin does not affect receptor binding but knocks out biological activity. Repeated injection of R128Q in normal C57BL/6J mice results in a progressive increase in body weight. This demonstrates that R128Q is able to interfere with the negative feedback control of endogenous leptin. This mutant could be of therapeutic use for wasting disorders, such as anorexia and cachexia, where weight gain would be beneficial. Leptin, a fat secreted hormone, regulates ingestive behaviour and energy balance by binding to a specific receptor. Using site-directed mutagenesis, we screened for single amino acid residues in human leptin which are critical for receptor binding and biological activity. Here we report that one of these mutants has in vivo antagonistic properties. An Arg to Gln substitution at position 128 of human leptin does not affect receptor binding but knocks out biological activity. Repeated injection of R128Q in normal C57BL/6J mice results in a progressive increase in body weight. This demonstrates that R128Q is able to interfere with the negative feedback control of endogenous leptin. This mutant could be of therapeutic use for wasting disorders, such as anorexia and cachexia, where weight gain would be beneficial. ©1997 Federation of European Biochemical Societies. © 1997 Federation of European Biochemical Societies. |
| Author | Plaetinck, Geert Devos, René Guisez, Yves Verploegen, Sandra A.B.W. Van der Heyden, José |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/9089297$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Anorexia Antagonist Body weight Cachexia Carrier Proteins - antagonists & inhibitors Humans Leptin Mice Mice, Inbred C57BL Mice, Obese Mutagenesis Mutagenesis, Site-Directed Mutation Obesity - chemically induced Proteins - genetics Receptors, Cell Surface Receptors, Leptin Selection, Genetic Weight Gain |
| Title | A human leptin mutant induces weight gain in normal mice |
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