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Cell Mol Neurobiol. 2010 Jan;30(1):23-33. doi: 10.1007/s10571-009-9427-x. Epub 2009 Jul 7.

Metabolic characterization of a mouse deficient in all known leptin receptor isoforms.

Author information

1
Molecular and Integrative Neurosciences Department, The Harold L. Dorris Neurological Research Institute, The Scripps Research Institute, La Jolla, CA 92037, USA. olivia1@scripps.edu

Abstract

We have characterized a newly generated mouse model of obesity, a mouse strain deficient in all five previously described leptin receptor isoforms. These transgenic mice, named the db (333)/db (333) mice, were identified from an ENU mutagenesis screen and carry a point mutation in the seventh exon of the db gene encoding the leptin receptor, resulting in a premature stop codon (Y(333)Stop) and gene product that lacks STAT signaling domains. db (333)/db (333) mice have a morbidly obese phenotype, with body weights diverging from wild type as early as 4 weeks of age (P < 0.05). To determine the contribution of the short isoforms of the leptin receptor in this metabolic phenotype, we performed an extensive metabolic characterization of the db (333)/db (333) mouse in relation to the well-characterized db/db mouse lacking only the long form of the leptin receptor. db (333)/db (333) mice have similar endocrine and metabolic parameters as previously described in other leptin receptor transgenic mice including db/db mice that lack only the long isoform of the leptin receptor. However, db (333)/db (333) mice show a subtle trend toward higher body weight and insulin levels, lower oxygen, carbon dioxide production, respiratory exchange ratio (RER), and temperature than db/db mice suggesting the short isoforms may play an additional role in energy homeostasis.

PMID:
19582570
PMCID:
PMC2813927
DOI:
10.1007/s10571-009-9427-x
[Indexed for MEDLINE]
Free PMC Article

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