Guest guest Posted July 25, 2002 Report Share Posted July 25, 2002 Another source of leptin .- Brad with respect to change and species survival I agree, changes means protein transcription diferences and adaptatives one's. You know, what not kill's you make's you strong. Regards Letter Nature Medicine 10, 739 - 743 (2004) Published online: 20 June 2004; | doi:10.1038/nm1071 Socs3 deficiency in the brain elevates leptin sensitivity and confers resistance to diet-induced obesityHiroyuki Mori1, Reiko Hanada2, Toshikatsu Hanada1, Daisuke Aki1, Ryuichi Mashima1, Hitomi Nishinakamura1, Takehiro Torisu1, R Chien3, Hideo Yasukawa4 & Akihiko Yoshimura1 1 Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. 2 Department of Molecular Genetics, Institute of Life Science, Kurume University, 2432-3 Aikawa-machi, Kurume 839-0861, Japan. 3 Institute of Molecular Medicine and Department of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, California 92093-0641, USA. 4 Cardiovascular Research Institute and The Third Department of Internal Medicine, Kurume University, 67 Asahi-machi, Kurume 830-0011, Japan.Correspondence should be addressed to Akihiko Yoshimura yakihiko@... Leptin is an adipocyte-derived hormone that plays a key role in energy homeostasis, yet resistance to leptin is a feature of most cases of obesity in humans and rodents. In vitro analysis suggested that the suppressor of cytokine signaling-3 (Socs3) is a negative-feedback regulator of leptin signaling involved in leptin resistance. To determine the functional significance of Socs3 in vivo, we generated neural cell–specific SOCS3 conditional knockout mice using the Cre–loxP system. Compared to their wild-type littermates, Socs3-deficient mice showed enhanced leptin-induced hypothalamic Stat3 tyrosine phosphorylation as well as pro-opiomelanocortin (POMC) induction, and this resulted in a greater body weight loss and suppression of food intake. Moreover, the Socs3-deficient mice were resistant to high fat diet–induced weight gain and hyperleptinemia, and insulin-sensitivity was retained. These data indicate that Socs3 is a key regulator of diet-induced leptin as well as insulin resistance. Our study demonstrates the negative regulatory role of Socs3 in leptin signaling in vivo, and thus suppression of Socs3 in the brain is a potential therapy for leptin-resistance in obesity. MORE ARTICLES LIKE THISThese links to content published by NPG are automatically generated REVIEWSSuppressors of cytokine signaling and immunityNature Immunology Review (01 Dec 2003) See all 6 matches for Reviews NEWS AND VIEWSMatching SOCS with functionNature Immunology News and Views (01 Jun 2003) RESEARCHEnhanced leptin sensitivity and attenuation of diet-induced obesity in mice with haploinsufficiency of Socs3Nature Medicine Letters (01 Jul 2004)SOCS3 negatively regulates IL-6 signaling in vivoNature Immunology Article (01 Jun 2003)IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophagesNature Immunology Article (01 Jun 2003) See all 13 matches for Research Top ABSTRACT Previous | Next Table of contents Full text Download PDF Send to a friend Figures & Tables Supplementary info Export citation ADVERTISEMENT ISSN: 1078-8956EISSN: 1546-170X Journal home | Advance online publication | Current issue | Archive | Press releases | Focuses | For authors | Online submission | Permissions | For referees | Free online issue | About the journal | Contact the journal | Subscribe | Advertising | work@npg | naturereprints | About this site | For librarians ©2004 Nature Publishing Group | Privacy policy Quote Link to comment Share on other sites More sharing options...
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