TY - JOUR
T1 - Transgenic expression of syndecan-1 uncovers a physiological control of feeding behavior by syndecan-3
AU - Reizes, Ofer
AU - Lincecum, John
AU - Wang, Zihua
AU - Goldberger, Olga
AU - Huang, Li
AU - Kaksonen, Marko
AU - Ahima, Rexford
AU - Hinkes, Michael T.
AU - Barsh, Gregory S.
AU - Rauvala, Heikki
AU - Bernfield, Merton
N1 - Funding Information:
The authors would like to thank members of the Bernfield laboratory and Dr. Joseph A. Majzoub for advice, input, and critical reading of the manuscript. We would also like to thank Sharlene Yang for excellent technical assistance and Karen Strehlow for her initial work on the syndtrophin mice. This work was supported by grants from the National Institutes of Health (NIH) to M.B. (HD06763), J. Volpe (HD18655), G.S.B. (DK28506), and from the Academy of Finland and the Technical Research Centre of Finland (Program of Molecular Neurobiology), and the Sigrid Juselius Foundation to H.K. G.S.B. is an Associate Investigator of the Howard Hughes Medical Institute. O.R. was supported by an individual NRSA from the NIH.
PY - 2001/7/13
Y1 - 2001/7/13
N2 - 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 α melanocyte stimulating hormone (αMSH). Via their HS chains, syndecans potentiate the action of agouti-related protein and agouti signaling protein, endogenous inhibitors of αMSH. 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.
AB - 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 α melanocyte stimulating hormone (αMSH). Via their HS chains, syndecans potentiate the action of agouti-related protein and agouti signaling protein, endogenous inhibitors of αMSH. 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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U2 - 10.1016/S0092-8674(01)00415-9
DO - 10.1016/S0092-8674(01)00415-9
M3 - Article
C2 - 11461706
AN - SCOPUS:17844372731
SN - 0092-8674
VL - 106
SP - 105
EP - 116
JO - Cell
JF - Cell
IS - 1
ER -