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Leptin and Obesity Associated Diseases
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Leptin and Obesity Associated Diseases

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: 15 July 2024 | Viewed by 1910

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,

Leptin was discovered almost 30 years ago as a lipostatic signal produced by adipocytes to inform the central nervous system about energy stores in order to control body weight. However, leptin was found to be a pleiotropic hormone with many different effects in multiple systems in addition to human metabolism, such as reproduction, including pregnancy (trophoblast is the second source of leptin); immunological functions; and cardiovascular and musculoskeletal systems (muscle is the third source of leptin).

Furthermore, leptin levels are increased in obesity, and may mediate, at least in part, the pathophysiological complications of being overweight; therefore, leptin may also be considered as a link between obesity and its associated diseases, such as diabetes, cardiovascular disease, musculoskeletal problems, and immunological diseases, both immune deficiency- and inflammation-related diseases. This refers not only to autoimmune diseases, but also concerns cancer development and progression.

The aim of this Special Issue is to provide a specialized forum which can summarize and further enlarge the knowledge of leptin in the pathophysiology of obesity-associated diseases.

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

  • Leptin and immunometabolism;
  • Leptin and diabetes;
  • Leptin and cardiovascular disease;
  • Leptin and musculoskeletal diseases
  • Leptin and fertility;
  • Leptin and pathological pregnancy;
  • Leptin and autoimmune diseases;
  • 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
  • obesity
  • obesity-associated disease
  • inflammation

Published Papers (2 papers)

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15 pages, 816 KiB  
Article
The Metabolically Obese, Normal-Weight Phenotype in Young Rats Is Associated with Cognitive Impairment and Partially Preventable with Leptin Intake during Lactation
by Margalida Cifre, Andreu Palou and Paula Oliver
Int. J. Mol. Sci. 2024, 25(1), 228; https://doi.org/10.3390/ijms25010228 - 22 Dec 2023
Viewed by 1029
Abstract
The intake of high-fat diets (HFDs) and obesity are linked to cognitive impairment. Here, we aimed to investigate whether an early metabolically obese, normal-weight (MONW) phenotype, induced with an HFD in young rats, also leads to cognitive dysfunction and to evaluate the potential [...] Read more.
The intake of high-fat diets (HFDs) and obesity are linked to cognitive impairment. Here, we aimed to investigate whether an early metabolically obese, normal-weight (MONW) phenotype, induced with an HFD in young rats, also leads to cognitive dysfunction and to evaluate the potential cognitive benefits of neonatal intake of leptin. To achieve this, Wistar rats orally received physiological doses of leptin or its vehicle during lactation, followed by 11 weeks of pair-feeding with an HFD or control diet post-weaning. Working memory was assessed using a T-maze, and gene expression in the hippocampus and peripheral blood mononuclear cells (PBMCs) was assessed with real-time RT-qPCR to identify cognition biomarkers. Young MONW-like rats showed hippocampal gene expression changes and decreased working memory. Animals receiving leptin during lactation presented similar gene expression changes but preserved working memory despite HFD intake, partly due to improved insulin sensitivity. Notably, PBMC Syn1 expression appears as an accessible biomarker of cognitive health, reflecting both the detrimental effect of HFD intake at early ages despite the absence of obesity and the positive effects of neonatal leptin treatment on cognition. Thus, the MONW phenotype developed at a young age is linked to cognitive dysfunction, which is reflected at the transcriptomic level in PBMCs. Neonatal leptin intake can partly counteract this impaired cognition resulting from early HFD consumption. Full article
(This article belongs to the Special Issue Leptin and Obesity Associated Diseases)
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Review

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13 pages, 670 KiB  
Review
Gestational Weight Gain: Is the Role of Genetic Variants a Determinant? A Review
by Reyna Sámano, Hugo Martínez-Rojano, Gabriela Chico-Barba, Ricardo Gamboa, María Eugenia Mendoza-Flores, Francisco Javier Robles-Alarcón, Itzel Pérez-Martínez and Irma Eloisa Monroy-Muñoz
Int. J. Mol. Sci. 2024, 25(5), 3039; https://doi.org/10.3390/ijms25053039 - 06 Mar 2024
Viewed by 513
Abstract
Excessive or insufficient gestational weight gain (GWG) leads to diverse adverse maternal and neonatal outcomes. There is evidence that pregestational body mass index (pBMI) plays a role in GWG, but no genetic cause has been identified. In this review, we aim to analyze [...] Read more.
Excessive or insufficient gestational weight gain (GWG) leads to diverse adverse maternal and neonatal outcomes. There is evidence that pregestational body mass index (pBMI) plays a role in GWG, but no genetic cause has been identified. In this review, we aim to analyze genotype variants associated with GWG. Results: We identified seven genotype variants that may be involved in GWG regulation that were analyzed in studies carried out in Brazil, Romania, the USA, Turkey, Ukraine, and Canada. Some genetic variants were only associated with GWG in certain races or depending on the pBMI. In women who were obese or overweight before gestation, some genetic variants were associated with GWG. Environmental and genetic factors together showed a greater association with GWG than genetic factors alone; for example, type of diet was observed to have a significant influence. Conclusions: We found little scientific evidence of an association between genotype variants in countries with a high prevalence of women of reproductive age who are overweight and obese, such as in Latin America. GWG may be more dependent on environmental factors than genetic variants. We suggest a deeper study of genetic variants, cytokines, and their possible association with GWG, always with the respective control of potential cofounding factors, such as pBMI, diet, and race. Full article
(This article belongs to the Special Issue Leptin and Obesity Associated Diseases)
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