Academic Journal
Leptin: 30 Years Later.
| Τίτλος: | Leptin: 30 Years Later. |
|---|---|
| Συγγραφείς: | Ahima RS; Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA., Flier JS; Department of Physiology and Department of Medicine, Harvard Medical School, Boston, Masschusetts, USA; email: Jeffrey_Flier@hms.harvard.edu. |
| Πηγή: | Annual review of physiology [Annu Rev Physiol] 2026 Feb; Vol. 88 (1), pp. 229-250. Date of Electronic Publication: 2025 Oct 03. |
| Τύπος έκδοσης: | Journal Article; Review |
| Γλώσσα: | English |
| Στοιχεία περιοδικού: | Publisher: Annual Reviews Country of Publication: United States NLM ID: 0370600 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1545-1585 (Electronic) Linking ISSN: 00664278 NLM ISO Abbreviation: Annu Rev Physiol Subsets: MEDLINE |
| Imprint Name(s): | Publication: Palo Alto Ca : Annual Reviews Original Publication: Palo Alto, Calif., Annual Reviews, inc. |
| Ιατρικοί όροι (MeSH): | Leptin*/physiology , Leptin*/deficiency , Leptin*/genetics , Leptin*/metabolism , Leptin*/therapeutic use, Obesity/physiopathology ; Obesity/metabolism ; Signal Transduction/physiology ; Receptors, Leptin/physiology ; Energy Metabolism/physiology ; Humans ; Animals ; Mice ; History, 21st Century |
| Περίληψη: | The discovery of leptin as an adipocyte-secreted hormone encoded by the ob gene whose absence produces severe obesity that is corrected by leptin repletion in both mice and humans was a transformative event in metabolic science. Leptin's discovery in 1994 accelerated the identification of central neuronal circuitry responsive to peripheral signals that regulate energy balance as well as metabolic, neuroendocrine, and other vital functions. Leptin's primary physiological role was initially viewed as preventing obesity by its levels rising, but subsequent research has emphasized the key role of falling levels to signal starvation. Resistance to leptin action, though partial, characterizes common forms of obesity. Despite much being learned about leptin signal transduction over 30 years, the precise molecular mechanisms for leptin resistance and common obesity remain unclear. Leptin therapy is effective in rare patients with congenital leptin deficiency and other low leptin conditions but not common obesity. Interestingly, reducing hyperleptinemia may prove useful in treating common obesity. |
| Contributed Indexing: | Keywords: adipose tissue; immunity; leptin; metabolism; neuroendocrine; obesity |
| Substance Nomenclature: | 0 (Leptin) 0 (Receptors, Leptin) |
| Entry Date(s): | Date Created: 20251003 Date Completed: 20260210 Latest Revision: 20260702 |
| Update Code: | 20260703 |
| DOI: | 10.1146/annurev-physiol-042324-100259 |
| PMID: | 41043250 |
| Βάση Δεδομένων: | MEDLINE |
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