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Leptin 2.0
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Leptin 2.0

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

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 12411

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
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Twenty five years ago, an important element in the regulation of weight was discovered: leptin. It was recognized as the adipocyte signal that informs the brain about fat stores, and it had been searched for for a long time. Thus, leptin could explain obesity as a failure of communication between fat and brain, either by leptin or leptin receptor mutation. However, soon after, leptin was found to be the first described adipokine that mediates the inflammatory state of obesity. In fact, leptin receptors and signalling share many features of of inflammatory cytokines. Thus, leptin has been found to be the cornerstone of immunometabolism, and there is a link between obesity and many associated pathophysiological conditions, such as diabetes, cardiovascular diseases, autoimmune diseases, pathology of reproduction and pregnancy, and cancer.  

The aim of this Special Issue is to summarize the knowledge of leptin function and its role in the pathophysiology of obesity-associated diseases at the molecular level.

Topics of the Special Issue include but are not limited to the following:

  • Leptin structure and its importance for brain functioning;
  • Leptin expression regulation;
  • Leptin receptor structure and isoforms;
  • Leptin receptor expression regulation;
  • Leptin and leptin receptor mutations and polymorphisms;
  • Leptin and immunometabolism;
  • Leptin and diabetes;
  • Leptin and cardiovascular disease;
  • Leptin and autoimmune diseases;
  • Leptin and reproduction;
  • Leptin and cancer.

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
  • obesity
  • immunometabolism
  • obesity associated pathology

Published Papers (3 papers)

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Research

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15 pages, 1839 KiB  
Article
Leptin Protein Expression and Promoter Methylation in Ovarian Cancer: A Strong Prognostic Value with Theranostic Promises
by Mourad Assidi, Fatimah M. Yahya, Maryam H. Al-Zahrani, Razan Elkhatib, Ali Zari, Aisha Elaimi, Jaudah Al-Maghrabi, Ashraf Dallol, Abdelbaset Buhmeida and Muhammad Abu-Elmagd
Int. J. Mol. Sci. 2021, 22(23), 12872; https://doi.org/10.3390/ijms222312872 - 28 Nov 2021
Cited by 9 | Viewed by 2321
Abstract
Ovarian cancer (OC) is the deadliest among all gynecological cancers. Epidemiological studies showed that obesity might influence many cancers including OC. One of the key factors that may link obesity and OC is leptin (LEP), known as an adipokine with pleiotropic effects on [...] Read more.
Ovarian cancer (OC) is the deadliest among all gynecological cancers. Epidemiological studies showed that obesity might influence many cancers including OC. One of the key factors that may link obesity and OC is leptin (LEP), known as an adipokine with pleiotropic effects on body homeostasis. This study aims to investigate the expression pattern of LEP, assess the methylation profiles of LEP and their associations with clinicopathological features including survival outcomes of OC patients. The protein expression of LEP was evaluated in 208 samples using both tissue microarray and immunohistochemistry techniques. The methylation profiles of LEP were measured in 63 formalin-fixed, paraffin-embedded tumor tissues by quantitative polymerase chain reaction using a MethyLight assay. Our results showed a significant association of LEP protein overexpression with several clinicopathological variables, mainly tumor subtype, LVI, age of menarche, tumor size and stage (p < 0.04). Kaplan–Meier analysis (using low expression versus high expression as a discriminator) indicated that LEP protein overexpression is a powerful positive prognosticator of both OC recurrence (DFS) and disease-specific survival (DSS) in our OC cohort (log-rank p = 0.01 and p = 0.002, respectively). This implies that patients with high LEP expression profiles live longer with less recurrence rates. Methylation analysis results demonstrated a clear association between no/low LEP protein expression pattern (38%) and LEP promoter CpG island hypermethylation (43%). Results of this study suggest that LEP is a powerful prognosticator of OC recurrence and DSS. LEP expression in OC seems to be regulated by its promoter hypermethylation through gene partial/total silencing. Further multi-institutional studies using larger cohorts are required to demystify the intricate molecular functions of this leptin-driven effects in OC pathophysiology and to accurately assess its theranostic potential and validate its prognostic/predictive power in OC onset, progression towards more effective and personalized management of OC patients. Full article
(This article belongs to the Special Issue Leptin 2.0)
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Review

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22 pages, 1381 KiB  
Review
Obesity as a Risk Factor for Dementia and Alzheimer’s Disease: The Role of Leptin
by Juan Antonio Flores-Cordero, Antonio Pérez-Pérez, Carlos Jiménez-Cortegana, Gonzalo Alba, Alfonso Flores-Barragán and Víctor Sánchez-Margalet
Int. J. Mol. Sci. 2022, 23(9), 5202; https://doi.org/10.3390/ijms23095202 - 6 May 2022
Cited by 50 | Viewed by 7252
Abstract
Obesity is a growing worldwide health problem, affecting many people due to excessive saturated fat consumption, lack of exercise, or a sedentary lifestyle. Leptin is an adipokine secreted by adipose tissue that increases in obesity and has central actions not only at the [...] Read more.
Obesity is a growing worldwide health problem, affecting many people due to excessive saturated fat consumption, lack of exercise, or a sedentary lifestyle. Leptin is an adipokine secreted by adipose tissue that increases in obesity and has central actions not only at the hypothalamic level but also in other regions and nuclei of the central nervous system (CNS) such as the cerebral cortex and hippocampus. These regions express the long form of leptin receptor LepRb, which is the unique leptin receptor capable of transmitting complete leptin signaling, and are the first regions to be affected by chronic neurocognitive deficits, such as mild cognitive impairment (MCI) and Alzheimer’s Disease (AD). In this review, we discuss different leptin resistance mechanisms that could be implicated in increasing the risk of developing AD, as leptin resistance is frequently associated with obesity, which is a chronic low-grade inflammatory state, and obesity is considered a risk factor for AD. Key players of leptin resistance are SOCS3, PTP1B, and TCPTP whose signalling is related to inflammation and could be worsened in AD. However, some data are controversial, and it is necessary to further investigate the underlying mechanisms of the AD-causing pathological processes and how altered leptin signalling affects such processes. Full article
(This article belongs to the Special Issue Leptin 2.0)
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11 pages, 890 KiB  
Review
Leptin in Dental Pulp and Periapical Tissues: A Narrative Review
by Jenifer Martin-Gonzalez, Juan J. Segura-Egea, Antonio Pérez-Pérez, Daniel Cabanillas-Balsera and Víctor Sánchez-Margalet
Int. J. Mol. Sci. 2022, 23(4), 1984; https://doi.org/10.3390/ijms23041984 - 11 Feb 2022
Cited by 3 | Viewed by 2321
Abstract
Leptin is a non-glycosylated 16 kDa protein synthesized mainly in adipose cells. The main function of leptin is to regulate energy homeostasis and weight control in a central manner. There is increasing evidence that leptin also has systemic effects, acting as a link [...] Read more.
Leptin is a non-glycosylated 16 kDa protein synthesized mainly in adipose cells. The main function of leptin is to regulate energy homeostasis and weight control in a central manner. There is increasing evidence that leptin also has systemic effects, acting as a link between innate and acquired immune responses. The expression of leptin and its receptor in human dental pulp and periradicular tissues have already been described, as well as several stimulatory effects of leptin protein expression in dental and periodontal tissues. The aim of this paper was to review and to compile the reported scientific literature on the role and effects of leptin in the dental pulp and periapical tissues. Twelve articles accomplished the inclusion criteria, and a comprehensive narrative review was carried out. Review of the available scientific literature concluded that leptin has the following effects on pulpal and periapical physiology: 1) Stimulates odontogenic differentiation of dental pulp stem cells (DPSCs), 2) Increases the expression of dentin sialophosphoprotein (DSPP) and dentin matrix protein-1 (DMP-1), odontoblastic proteins involved in odontoblastic differentiation and dentin mineralization, 3) Stimulates vascular endothelial growth factor (VEGF) expression in human dental pulp tissue and primary cultured cells of human dental pulp (hDPCs), 4) Stimulates angiogenesis in rat dental pulp cells, and 5) Induces the expression of interleucinas 6 and 8 in human periodontal ligament cells (hPDLCs). There is evidence which suggests that leptin is implicated in the dentin mineralization process and in pulpal and periapical inflammatory and reparative responses. Full article
(This article belongs to the Special Issue Leptin 2.0)
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