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Scientific article
Open access
English

Enhanced leptin sensitivity and improved glucose homeostasis in mice lacking suppressor of cytokine signaling-3 in POMC-expressing cells

Published inCell metabolism, vol. 4, no. 2, p. 123-132
Publication date2006-08
Abstract

Suppressor of cytokine signaling-3 (Socs-3) negatively regulates the action of various cytokines, as well as the metabolic hormones leptin and insulin. Mice with haploinsufficiency of Socs-3, or those with neuronal deletion of Socs-3, are lean and more leptin and insulin sensitive. To examine the role of Socs-3 within specific neurons critical to energy balance, we created mice with selective deletion of Socs-3 within pro-opiomelanocortin (POMC)-expressing cells. These mice had enhanced leptin sensitivity, measured by weight loss and food intake after leptin infusion. On chow diet, glucose homeostasis was improved despite normal weight gain. On a high-fat diet, the rate of weight gain was reduced, due to increased energy expenditure rather than decreased food intake; glucose homeostasis and insulin sensitivity were substantially improved. These studies demonstrate that Socs-3 within POMC neurons regulates leptin sensitivity and glucose homeostasis, and plays a key role in linking high-fat diet to disordered metabolism.

eng
Keywords
  • Animals
  • Cells, Cultured
  • Dietary Fats / pharmacology
  • Fatty Liver / prevention & control
  • Glucose / metabolism
  • Homeostasis
  • Leptin / pharmacology
  • Mice
  • Mice, Knockout
  • Pro-Opiomelanocortin / metabolism
  • Signal Transduction
  • Suppressor of Cytokine Signaling 3 Protein
  • Suppressor of Cytokine Signaling Proteins / genetics
  • Suppressor of Cytokine Signaling Proteins / metabolism
  • Weight Loss
Affiliation Not a UNIGE publication
Citation (ISO format)
KIEVIT, Paul et al. Enhanced leptin sensitivity and improved glucose homeostasis in mice lacking suppressor of cytokine signaling-3 in POMC-expressing cells. In: Cell metabolism, 2006, vol. 4, n° 2, p. 123–132. doi: 10.1016/j.cmet.2006.06.010
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Article (Published version)
accessLevelPublic
Identifiers
ISSN of the journal1550-4131
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