C
Christian Vaisse
Researcher at University of California, San Francisco
Publications - 76
Citations - 12766
Christian Vaisse is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Receptor & Gene. The author has an hindex of 41, co-authored 72 publications receiving 12061 citations. Previous affiliations of Christian Vaisse include University of California, Berkeley & University of Paris-Sud.
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Journal ArticleDOI
A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction
Karine Clément,Christian Vaisse,Najiba Lahlou,Sylvie Cabrol,Véronique Pelloux,Dominique Cassuto,Micheline Gourmelen,Christian Dina,Jean Chambaz,Jean-Marc Lacorte,Arnaud Basdevant,Pierre Bougnères,Yves Lebouc,Philippe Froguel,Bernard Guy-Grand +14 more
TL;DR: A homozygous mutation in the human leptin receptor gene results in a truncated leptin receptor lacking both the transmembrane and the intracellular domains, which indicates that leptin is an important physiological regulator of several endocrine functions in humans.
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Leptin regulation of bone resorption by the sympathetic nervous system and CART
Florent Elefteriou,Jong Deok Ahn,Shu Takeda,Michael Starbuck,Xiangli Yang,Xiuyun Liu,Hisataka Kondo,William G. Richards,Tony W. Bannon,Masaki Noda,Karine Clément,Christian Vaisse,Gerard Karsenty +12 more
TL;DR: This study establishes that leptin-regulated neural pathways control both aspects of bone remodelling, and demonstrates that integrity of sympathetic signalling is necessary for the increase in bone resorption caused by gonadal failure.
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Leptin activation of Stat3 in the hypothalamus of wild–type and ob/ob mice but not db/db mice
Christian Vaisse,Jeffrey L. Halaas,Curt M. Horvath,James E. Darnell,Markus Stoffel,Jeffrey M. Friedman +5 more
TL;DR: The data indicate the hypothalamus is a direct target of leptin action and that this activation is critically dependent on the gp-130-like leptin receptor isoform missing in C57BLKS/J db/db mice, the first in vivo demonstration of leptin signal transduction.
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A frameshift mutation in human MC4R is associated with a dominant form of obesity
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Melanocortin-4 receptor mutations are a frequent and heterogeneous cause of morbid obesity
Christian Vaisse,Karine Clément,Emmanuelle Durand,Serge Hercberg,Bernard Guy-Grand,Philippe Froguel +5 more
TL;DR: It is demonstrated that MC4-R mutations are a frequent but heterogeneous genetic cause of morbid obesity and transmission in the families of the carriers indicates a variable expressivity that is not related to the functional severity of the mutations.