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Advances in Leptin Biology
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Advances in Leptin Biology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 December 2025 | Viewed by 389

Special Issue Editor

Prof. Dr. Víctor Sánchez-Margalet

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, Hospital Universitario Virgen Macarena, Sevilla, Spain
Interests: leptin structure; leptin expression regulation; leptin receptor; leptin signaling; leptin action at central level; leptin as adipokine; leptin as a cornerstone of immunometabolism; leptin as link between obesity and associated pathophysiology, such as diabetes, cancer, rheumatologic diseases, or cardiovascular diseases
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Special Issue Information

Dear Colleagues,

Discovered three decades ago as a pivotal regulator of food intake and energy metabolism, leptin functions by linking peripheral adipose tissue with the central nervous system. Over the past 30 years, however, its role has expanded significantly, encompassing diverse physiological and pathological processes. The leptin receptor, expressed ubiquitously across tissues, highlights leptin's systemic influence. Deficiency in leptin or its receptor results in a range of pathophysiological consequences beyond obesity, including altered immune function, reproductive and cardiovascular dysfunctions, impaired glucose and bone mineral metabolism, and conflicting roles in cancer—acting as both a tumor promoter and a therapeutic response enhancer.

Leptin is now recognized as a cornerstone of immunometabolism, integral to regulating body weight, reproduction, and mediating various obesity-associated pathological conditions. These include leptin resistance or excess leading to diabetes, polycystic ovary syndrome (PCOS), infertility, immunodeficiencies, autoimmune diseases, inflammation, kidney and cardiovascular complications, and bone mass loss.

The goal of this Special Issue is to consolidate current knowledge about leptin's molecular functions and its contribution to the pathophysiology of diseases linked to obesity. Topics covered in the Special Issue include, but are not limited to:

  • The structure of leptin and its role in brain function;
  • Regulation of leptin expression;
  • The structure and isoforms of the leptin receptor;
  • Regulation of leptin receptor expression;
  • The mutations and polymorphisms of leptin and its receptor;
  • Leptin’s role in immunometabolism;
  • Leptin’s involvement in diabetes;
  • Leptin and its impact on cardiovascular disease;
  • Leptin’s relationship with autoimmune diseases;
  • Leptin’s role in reproduction;
  • Leptin and its influence on bone metabolism;
  • Leptin’s dual role in cancer development and therapeutic outcomes.

This Special Issue aims to provide a comprehensive overview of leptin’s multifaceted roles, advancing our understanding of its significance in both health and disease.

Prof. Dr. Víctor Sánchez-Margalet
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • leptin
  • leptin expression
  • leptin receptor
  • leptin action

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Published Papers (1 paper)

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Research

18 pages, 2924 KiB  
Article
Adoptive Transfer of Lepr+ Bone Marrow Cells Attenuates the Osteopetrotic Phenotype of db/db Mice
by Russell T. Turner, Carmen P. Wong, Kenneth A. Philbrick, Jessica A. Keune, Edwin M. Labut, Scott A. Menn, Adam J. Branscum and Urszula T. Iwaniec
Int. J. Mol. Sci. 2025, 26(11), 5120; https://doi.org/10.3390/ijms26115120 - 27 May 2025
Viewed by 193
Abstract
Leptin-deficient (ob/ob) and leptin receptor (Lepr)-deficient db/db mice develop a mild form of osteoclast-rich osteopetrosis, most evident in long bone epiphyses, implying leptin is important for normal replacement of cartilage during skeletal maturation. However, it is unclear [...] Read more.
Leptin-deficient (ob/ob) and leptin receptor (Lepr)-deficient db/db mice develop a mild form of osteoclast-rich osteopetrosis, most evident in long bone epiphyses, implying leptin is important for normal replacement of cartilage during skeletal maturation. However, it is unclear whether leptin acts as a permissive or regulatory factor and whether its actions are mediated via peripheral pathways. Here we show the osteopetrotic phenotype is not evident in ob/+ or db/+ mice, suggesting that leptin acts as a critical but permissive factor for skeletal maturation. The importance of leptin is further supported by our results showing that interventions known to increase bone resorption (mild cold stress, simulated microgravity, or particle-induced inflammation) did not advance skeletal maturation in ob/ob mice whereas long-duration hypothalamic leptin gene therapy was effective. Additionally, administration of leptin by subcutaneously implanted osmotic pumps (400 ng/h) for 2 weeks accelerated skeletal maturation in ob/ob mice. Because leptin has the potential to act on the skeleton through peripheral pathways, we interrogated osteoclast-lineage cells for the presence of Lepr and evaluated skeletal response to the introduction of bone marrow Lepr+ cells into db/db mice. We identified Lepr on marrow MCSFR+CD11b+ osteoclast precursors and on osteoclasts generated in vitro. We then adoptively transferred Lepr+ marrow cells from GFP mice or wildtype (WT) mice into Lepr- db/db mice. Following engraftment, most MCSFR+ CD11b+ cells in marrow expressed GFP. Whereas db/db→db/db had minimal influence on epiphyseal cartilage, WT→db/db decreased cartilage. These findings suggest peripheral leptin signaling is required for normal osteoclast-dependent replacement of cartilage by bone during skeletal maturation. Full article
(This article belongs to the Special Issue Advances in Leptin Biology)
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