Abstract
Leptin, which is secreted by adipocytes, the placenta and the stomach, not only controls appetite through leptin receptors in the hypothalamus but also regulates cell-mediated immunity. In this study we have demonstrated that continuous injection of leptin prevents the reduction in lymphocyte numbers normally observed in fasted and steroid-injected mice. Consistent with leptin-induced protection, we observed up-regulation of the bcl-xL gene as a result of signal transduction via leptin receptors on lymphocytes. We suggest that leptin might contribute to the recovery of immune suppression in malnourished mice by inhibiting lymphocyte apoptosis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects*
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Carrier Proteins / biosynthesis
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Carrier Proteins / genetics
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Cell Nucleus / ultrastructure
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DNA Fragmentation
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Fasting
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Female
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Hybridomas
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Hydrocortisone / antagonists & inhibitors
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Immunocompromised Host
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Leptin / genetics
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Leptin / pharmacology*
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Lymphocyte Count
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Proto-Oncogene Proteins c-bcl-2 / biosynthesis
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Proto-Oncogene Proteins c-bcl-2 / genetics
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RNA, Messenger / biosynthesis
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Receptors, Cell Surface*
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Receptors, Leptin
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T-Lymphocytes / immunology*
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T-Lymphocytes / ultrastructure
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bcl-X Protein
Substances
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Bcl2l1 protein, mouse
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Carrier Proteins
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Leptin
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Proto-Oncogene Proteins c-bcl-2
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RNA, Messenger
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Receptors, Cell Surface
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Receptors, Leptin
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bcl-X Protein
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leptin receptor, mouse
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Hydrocortisone