Combined neural inactivation of suppressor of cytokine signaling-3 and protein-tyrosine phosphatase-1B reveals additive, synergistic, and factor-specific roles in the regulation of body energy balance

Nadege Briancon, David E McNay, Eleftheria Maratos-Flier, Jeffrey S Flier

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

The adipokine hormone leptin triggers signals in the brain that ultimately lead to decreased feeding and increased energy expenditure. However, obesity is most often associated with elevated plasma leptin levels and leptin resistance. Suppressor of cytokine signaling (SOCS)-3 and protein-tyrosine phosphatase 1B (PTP-1B) are two endogenous inhibitors of tyrosine kinase signaling pathways and suppress both insulin and leptin signaling via different molecular mechanisms. Brain-specific inactivation of these genes individually in the mouse partially protects against diet-induced obesity (DIO) and insulin resistance. The aim of this study was to investigate possible genetic interactions between these two genes to determine whether combined reduction in these inhibitory activities results in synergistic, epistatic, or additive effects on energy balance control.
Original languageEnglish
Pages (from-to)3074-3084
Number of pages11
JournalDiabetes
Volume59
Issue number12
Early online date28 Sep 2010
DOIs
Publication statusPublished - Dec 2010

Keywords

  • animals
  • crosses, genetic
  • energy metabolism
  • female
  • insulin resistance
  • leptin
  • male
  • mice
  • mice, inbred C57BL
  • mice, knockout
  • mutation
  • obesity
  • protein tyrosine phosphatase, non-receptor type 1
  • suppressor of cytokine signaling proteins
  • weight gain

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