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Transgenic expression of syndecan-1 uncovers a physiological control of feeding behavior by syndecan-3.
Authors:O Reizes  J Lincecum  Z Wang  O Goldberger  L Huang  M Kaksonen  R Ahima  M T Hinkes  G S Barsh  H Rauvala  M Bernfield
Affiliation:Division of Newborn Medicine, Department of Pediatrics and Cell Biology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA. oreizes@go.com
Abstract:Transgenic expression in the hypothalamus of syndecan-1, a cell surface heparan sulfate proteoglycan (HSPG) and modulator of ligand-receptor encounters, produces mice with hyperphagia and maturity-onset obesity resembling mice with reduced action of alpha melanocyte stimulating hormone (alphaMSH). Via their HS chains, syndecans potentiate the action of agouti-related protein and agouti signaling protein, endogenous inhibitors of alphaMSH. In wild-type mice, syndecan-3, the predominantly neural syndecan, is expressed in hypothalamic regions that control energy balance. Food deprivation increases hypothalamic syndecan-3 levels several-fold. Syndecan-3 null mice, otherwise apparently normal, respond to food deprivation with markedly reduced reflex hyperphagia. We propose that oscillation of hypothalamic syndecan-3 levels physiologically modulates feeding behavior.
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