Abstract

The recent positional cloning of the mouse ob gene and its human homolog has provided the basis to investigate the potential role of the ob gene product in body weight regulation. A biologically active form of recombinant mouse OB protein was overexpressed and purified to near homogeneity from a bacterial expression system. Peripheral and central administration of microgram doses of OB protein reduced food intake and body weight of ob / ob and diet-induced obese mice but not in db / db obese mice. The behavioral effects after brain administration suggest that OB protein can act directly on neuronal networks that control feeding and energy balance.

Keywords

Recombinant DNAPeripheralSIGNAL (programming language)Artificial neural networkEndocrinologyInternal medicineChemistryBiologyNeuroscienceCell biologyMedicineBiochemistryComputer scienceArtificial intelligenceGene

MeSH Terms

AnimalsBrainDiabetes MellitusDietDose-Response RelationshipDrugEatingFemaleInjectionsIntraperitonealInjectionsIntravenousInjectionsIntraventricularLeptinMaleMiceMiceInbred AKRMiceInbred C57BLMiceObeseNerve NetObesityProteinsRecombinant ProteinsWeight Loss

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Publication Info

Year
1995
Type
article
Volume
269
Issue
5223
Pages
546-549
Citations
3253
Access
Closed

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Cite This

L. Arthur Campfield, Françoise J. Smith, Yves Guisez et al. (1995). Recombinant Mouse OB Protein: Evidence for a Peripheral Signal Linking Adiposity and Central Neural Networks. Science , 269 (5223) , 546-549. https://doi.org/10.1126/science.7624778

Identifiers

DOI
10.1126/science.7624778
PMID
7624778

Data Quality

Data completeness: 81%