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      Transcription Factor STAT3 in Leptin Target Neurons of the Rat Hypothalamus

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          Leptin is an adipose tissue-derived hormone that regulates body weight via interactions with hypothalamic neuronal circuitries expressing specific leptin receptors (Ob-R). The Ob-Rs act via the JAK-STAT (Janus kinase-signal transducers and activators of transcription) pathway of signal transduction. Recent evidence suggests that primarily the transcription factor STAT3 mediates leptin’s action in the hypothalamus. We have investigated the presence and cellular localization of STAT3 protein in the rat hypothalamus by means of indirect immunofluorescence histochemistry using a rabbit polyclonal STAT3 antiserum. The antiserum identified a 92-kDa protein using Western blotting on rat hypothalamic homogenates, corresponding to the expected size of STAT3. STAT3 immunoreactivity was demonstrated in Ob-R-containing neurons of the paraventricular nucleus (parvocellular part), periventricular nucleus, arcuate nucleus and in the lateral hypothalamic area. Direct double-labeling showed presence of STAT3 immunoreactivity in neuropeptide Y (NPY)-containing neurons of the ventromedial part of the arcuate nucleus and in proopiomelanocortin (POMC)-containing neurons of the ventrolateral part of the arcuate nucleus. The results provide an anatomical basis for a leptin action mediated by STAT3 in Ob-R-containing NPY and POMC neurons of the arcuate nucleus, as well as by Ob-R-containing neurons of the parvocellular paraventricular nucleus and lateral hypothalamic area.

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          Most cited references 8

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          Identification and expression cloning of a leptin receptor, OB-R.

          The ob gene product, leptin, is an important circulating signal for the regulation of body weight. To identify high affinity leptin-binding sites, we generated a series of leptin-alkaline phosphatase (AP) fusion proteins as well as [125I]leptin. After a binding survey of cell lines and tissues, we identified leptin-binding sites in the mouse choroid plexus. A cDNA expression library was prepared from mouse choroid plexus and screened with a leptin-AP fusion protein to identify a leptin receptor (OB-R). OB-R is a single membrane-spanning receptor most related to the gp130 signal-transducing component of the IL-6 receptor, the G-CSF receptor, and the LIF receptor. OB-R mRNA is expressed not only in choroid plexus, but also in several other tissues, including hypothalamus. Genetic mapping of the gene encoding OB-R shows that it is within the 5.1 cM interval of mouse chromosome 4 that contains the db locus.
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            Orexins and Orexin Receptors: A Family of Hypothalamic Neuropeptides and G Protein-Coupled Receptors that Regulate Feeding Behavior

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              Abnormal splicing of the leptin receptor in diabetic mice.

              Mutations in the mouse diabetes (db) gene result in obesity and diabetes in a syndrome resembling morbid human obesity. Previous data suggest that the db gene encodes the receptor for the obese (ob) gene product, leptin. A leptin receptor was recently cloned from choroid plexus and shown to map to the same 6-cM interval on mouse chromosome 4 as db. This receptor maps to the same 300-kilobase interval as db, and has at least six alternatively spliced forms. One of these splice variants is expressed at a high level in the hypothalamus, and is abnormally spliced in C57BL/Ks db/db mice. The mutant protein is missing the cytoplasmic region, and is likely to be defective in signal transduction. This suggests that the weight-reducing effects of leptin may be mediated by signal transduction through a leptin receptor in the hypothalamus.

                Author and article information

                S. Karger AG
                December 1998
                18 December 1998
                : 68
                : 6
                : 420-427
                Department of Neuroscience, Karolinska Institute, Stockholm, Sweden
                54392 Neuroendocrinology 1998;68:420–427
                © 1998 S. Karger AG, Basel

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                Page count
                Figures: 6, References: 38, Pages: 8
                Ontogeny and Regulation of Hypothalamic Neurons


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