The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Leptin, from fat to inflammation: old questions and new insights
Open accessAbstract
Leptin is 16 kDa adipokine that links nutritional status with neuroendocrine and immune functions. Initially thought to be a satiety factor that regulates body weight by inhibiting food intake and stimulating energy expenditure, leptin is a pleiotropic hormone whose multiple effects include regulation of endocrine function, reproduction, and immunity. Leptin can be considered as a pro‐inflammatory cytokine that belongs to the family of long‐chain helical cytokines and has structural similarity with interleukin‐6, prolactin, growth hormone, IL‐12, IL‐15, granulocyte colony‐stimulating factor and oncostatin M. Because of its dual nature as a hormone and cytokine, leptin links the neuroendocrine and the immune system. The role of leptin in the modulation of immune response and inflammation has recently become increasingly evident. The increase in leptin production that occurs during infection and inflammation strongly suggests that leptin is a part of the cytokine network which governs the inflammatory‐immune response and the host defense mechanisms. Leptin plays an important role in inflammatory processes involving T cells and has been reported to modulate T‐helper cells activity in the cellular immune response. Several studies have implicated leptin in the pathogenesis of autoimmune inflammatory conditions, such as experimental autoimmune encephalomyelitis, type 1 diabetes, rheumatoid arthritis, and intestinal inflammation. Very recently, a key role for leptin in osteoarthritis has been demonstrated: leptin indeed exhibits, in concert with other pro‐inflammatory cytokines, a detrimental effect on articular cartilage by promoting nitric oxide synthesis in chondrocytes. Here, we review the recent advances regarding leptin biology with a special focus on those actions relevant to the role of leptin in the pathophysiology of inflammatory processes and immune responses.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Positional cloning of the mouse obese gene and its human homologue
Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994) · Nature · doi:10.1038/372425a0 · Cited by 13,419
Role of leptin in the neuroendocrine response to fasting
Ahima, R. S., Prabakaran, D., Mantzoros, C., Qu, D., Lowell, B., Maratos-Flier, E., & Flier, J. S. (1996) · Nature · doi:10.1038/382250a0 · Cited by 3,117
Abnormal splicing of the leptin receptor in diabetic mice
Lee, G.-H., Proenca, R., Montez, J. M., Carroll, K. M., Darvishzadeh, J. G., Lee, J. I., & Friedman, J. M. (1996) · Nature · doi:10.1038/379632a0 · Cited by 2,327
Dimerization of cell surface receptors in signal transduction
Heldin, C.-H. (1995) · Cell · doi:10.1016/0092-8674(95)90404-2 · Cited by 1,634
A leptin missense mutation associated with hypogonadism and morbid obesity
Strobel, A., Issad, T., Camoin, L., Ozata, M., & Strosberg, A. D. (1998) · Nature Genetics · doi:10.1038/ng0398-213 · Cited by 1,158
STAT3 signalling is required for leptin regulation of energy balance but not reproduction
Bates, S. H., Stearns, W. H., Dundon, T. A., Schubert, M., Tso, A. W. K., Wang, Y., Banks, A. S., Lavery, H. J., Haq, A. K., Maratos-Flier, E., et al. (2003) · Nature · doi:10.1038/nature01388 · Cited by 1,010 · cited 1×
“in the Y1138S knock-in mouse, so implying a STAT3-independent leptin receptor signaling transduction pathway [51,52].”
BackgroundThe weight of leptin in immunity
Cava, A. L., & Matarese, G. (2004) · Nature Reviews Immunology · doi:10.1038/nri1350 · Cited by 927 · cited 3×
“Acknowledgements: We thank Dr. G. Matarese for his helpful advices and for his continued support.”
BackgroundInfluentialDivergent Signaling Capacities of the Long and Short Isoforms of the Leptin Receptor
Bjørbæk, C., Uotani, S., da Silva, B., & Flier, J. S. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.51.32686 · Cited by 890
Activation of Downstream Signals by the Long Form of the Leptin Receptor
Banks, A. S., Davis, S. M., Bates, S. H., & Myers, M. G. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.19.14563 · Cited by 797
Sarraf, P., Frederich, R. C., Turner, E. M., Ma, G., Jaskowiak, N. T., Rivet, D. J., Flier, J. S., Lowell, B. B., Fraker, D. L., & Alexander, H. R. (1997) · The Journal of Experimental Medicine · doi:10.1084/jem.185.1.171 · Cited by 791
Cited by
Adipokines as emerging mediators of immune response and inflammation
Lago, F., Dieguez, C., Gómez-Reino, J., & Gualillo, O. (2007) · Nature Clinical Practice Rheumatology · doi:10.1038/ncprheum0674 · Cited by 567
Self-citationMechanisms of β-Cell Death in Type 2 Diabetes
Donath, M. Y., Ehses, J. A., Maedler, K., Schumann, D. M., Ellingsgaard, H., Eppler, E., & Reinecke, M. (2005) · Diabetes · doi:10.2337/diabetes.54.suppl_2.s108 · Cited by 444
Islet Inflammation in Type 2 Diabetes
Donath, M. Y., Schumann, D. M., Faulenbach, M., Ellingsgaard, H., Perren, A., & Ehses, J. A. (2008) · Diabetes Care · doi:10.2337/dc08-s243 · Cited by 334
Role of Leptin in Inflammation and Vice Versa
Pérez-Pérez, A., Sánchez-Jiménez, F., Vilariño-García, T., & Sánchez-Margalet, V. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21165887 · Cited by 330
Inflammatory Process in Type 2 Diabetes: The Role of Cytokines
ALEXANDRAKI, K., PIPERI, C., KALOFOUTIS, C., SINGH, J., ALAVERAS, A., & KALOFOUTIS, A. (2006) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1372.039 · Cited by 309
Metadata
- Authors
- Otero, M., Lago, R., Lago, F., Casanueva, F. F., Dieguez, C., Gómez-Reino, J. J., & Gualillo, O.
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2004-12-08
- Volume
- 579
- Issue
- 2
- Pages
- 295-301
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2012951157
- Cited by
- 409
- References
- 13
- FWCI
- 19.58
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Leptin, from fat to inflammation: old questions and new insights. https://app.cochat.ai/papers/10.1016/j.febslet.2004.11.024
- The paper
- Otero, M., Lago, R., Lago, F., Casanueva, F. F., Dieguez, C., Gómez-Reino, J. J., & Gualillo, O. (2005). Leptin, from fat to inflammation: old questions and new insights. FEBS Letters. https://doi.org/10.1016/j.febslet.2004.11.024
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.