Monogenic models of obesity

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The study of rodent monogenic models of obesity has yielded significant insights into the pathogenesis of obesity. Multiple independent mutations in several genes can produce obesity. As these genes act in different regulatory pathways, it is clear that multiple mechanisms can produce obesity. Furthermore, a single gene defect can produce regulatory deficits in multiple modes of energy expenditure. The most severe forms of genetic obesity involve multiple pathogenic processes. It is significant that regulatory defects in any single component of caloric intake or energy expenditure appear to be sufficient to produce obesity. Finally, the systems regulating energy balance are loosely coupled; positive and negative influences are not completely balanced, both in strength as well as temporally.

Original languageEnglish (US)
Pages (from-to)277-284
Number of pages8
JournalBehavior Genetics
Volume27
Issue number4
DOIs
StatePublished - 1997
Externally publishedYes

Fingerprint

obesity
Obesity
energy expenditure
Energy Metabolism
defect
expenditure
gene
Inborn Genetic Diseases
genes
Energy Intake
energy balance
rodent
Genes
energy
mutation
Rodentia
energy intake
rodents
pathogenesis
Mutation

Keywords

  • Monogenic models
  • Obesity

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)
  • Behavioral Neuroscience
  • Psychology(all)

Cite this

Monogenic models of obesity. / Chua, Jr., Streamson C.

In: Behavior Genetics, Vol. 27, No. 4, 1997, p. 277-284.

Research output: Contribution to journalArticle

Chua, Jr., Streamson C. / Monogenic models of obesity. In: Behavior Genetics. 1997 ; Vol. 27, No. 4. pp. 277-284.
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