Abstract

The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.

Keywords

ObesityAdipose tissueGenePositional cloningCloning (programming)EndocrinologyBiologyMutationGene productEnergy expenditureInternal medicineGeneticsMedicineGene expressionMutant

MeSH Terms

Adipose TissueAmino Acid SequenceAnimalsBase SequenceChromosome MappingChromosomesArtificialYeastCloningMolecularConserved SequenceCrossesGeneticExonsHumansMiceMiceInbred C57BLMiceInbred DBAMiceObeseMolecular Sequence DataObesityRNAMessenger

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Publication Info

Year
1994
Type
article
Volume
372
Issue
6505
Pages
425-432
Citations
13270
Access
Closed

External Links

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13270
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Cite This

Yiying Zhang, Ricardo Proenca, Margherita Maffei et al. (1994). Positional cloning of the mouse obese gene and its human homologue. Nature , 372 (6505) , 425-432. https://doi.org/10.1038/372425a0

Identifiers

DOI
10.1038/372425a0
PMID
7984236

Data Quality

Data completeness: 81%