Special Issue "Molecular Mechanisms Underlying Eating Disorders and Obesity"

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 11422

Special Issue Editors

School of Pharmacy, University of Camerino, 62032 Camerino, Italy
Interests: eating disorders; binge eating; obesity; pharmacology; behavioral neuroscience; neurobiology of food and drug addiction; epigenetics; stress
Faculty of Bioscience and Technology for Food Agriculture and Environment, University of Teramo, Via Balzarini, Teramo, Italy
Interests: molecular mechanisms; epigenetics; gene expression; DNA methylation; biomarkers; endocannabinoids

Special Issue Information

Dear Colleagues,

Eating disorders (EDs) and obesity represent an urgent public health problem; although they appear as entirely separate, they share many similarities. Core symptoms are problematic eating habits and the inability to control body weight and food consumption; furthermore, it is well established that obesity can contribute to ED behaviors and vice-versa. A combination of environmental, nutritional and genetic factors defines individual predisposition to develop these conditions but, despite the well-recognized role of all these factors, the interaction among diet habits, environmental and heritable factors in the development of EDs and obesity is still largely unexplored.

In the last decade, a lot of progress has been made in identifying molecular targets, as well as mechanisms underlying their transcriptional regulation, potentially involved in the development and progression of EDs and obesity.

This Special Issue aims to highlight recent advances made in this field that are useful to prevent the individual risk of developing an ED and obesity, as well as to provide invaluable help for the advancement of preventive and pharmacotherapy strategies with the assessment of novel effective molecular targets.

We encourage researchers interested in these topics to present original research articles, emphasizing current preclinical and clinical knowledge on the molecular mechanisms underlying the regulation of specific targets involved in the development, progression or treatment of obesity and EDs. Moreover, critically and systematically, review articles, covering the related research, providing concluding remarks and an outlook, will be considered for inclusion in this Special Issue.

Dr. Maria Vittoria Micioni Di Bonaventura
Dr. Mariangela Pucci
Guest Editors

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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • obesity
  • eating disorders
  • stress
  • diet
  • environmental factors
  • reward system
  • epigenetic
  • biomarkers
  • new targets for treatment

Published Papers (5 papers)

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Research

Jump to: Review

14 pages, 1517 KiB  
Article
Relationship between Liver Stiffness and Steatosis in Obesity Conditions: In Vivo and In Vitro Studies
Biomolecules 2022, 12(5), 733; https://doi.org/10.3390/biom12050733 - 23 May 2022
Cited by 6 | Viewed by 2296
Abstract
Obesity is a major risk factor for metabolic dysfunction such as non-alcoholic fatty liver disease (NAFLD). The NAFLD spectrum ranges from simple steatosis, to steatohepatitis, fibrosis, and cirrhosis. The aim of this study is to characterize the grade of steatosis being associated with [...] Read more.
Obesity is a major risk factor for metabolic dysfunction such as non-alcoholic fatty liver disease (NAFLD). The NAFLD spectrum ranges from simple steatosis, to steatohepatitis, fibrosis, and cirrhosis. The aim of this study is to characterize the grade of steatosis being associated with overnutrition and obesity, both at the level of single hepatocyte and whole liver, and to correlate it with the hepatocyte/liver stiffness and dysfunction. For the in vivo study, 60 subjects were enrolled and grouped based on the stage of liver steatosis/fibrosis according to biochemical analyses, liver ultrasonography (USG) and acoustic radiation force impulse shear wave elastography (ARFI-SWE). For single hepatocyte analyses we employed in vitro models of moderate and severe steatosis on which to assess the single cell biomechanics by Single Cell Force Spectroscopy (SCFS) and Quantitative Phase Microscopy (QPM). Results show that in vivo liver stiffness depends mainly on the extent of fat accumulation and not on fibrosis. These results parallel the in vitro observations showing that hepatocyte stiffness and dysfunction increase with increasing fat accumulation and lipid droplet enlargement. Our findings indicate that the extent of steatosis markedly affects the biomechanical properties of both liver and single hepatocytes thus proving insights about the role of modulation of liver/hepatocyte elasticity as a physical mechanism transducing the obesity-dependent excess of plasmatic lipids towards liver steatosis and dysfunction. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Eating Disorders and Obesity)
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18 pages, 3878 KiB  
Article
Anti-Obesity Effect of α-Cubebenol Isolated from Schisandra chinensis in 3T3-L1 Adipocytes
Biomolecules 2021, 11(11), 1650; https://doi.org/10.3390/biom11111650 - 08 Nov 2021
Cited by 4 | Viewed by 1885
Abstract
The efficacy of α-cubebenol isolated from Schisandra chinensis has been studied in several diseases, including cecal ligation, puncture challenge-induced sepsis, and degranulation of neutrophils. To identify the novel functions of α-cubebenol on lipid metabolism, alterations on the regulation of lipogenesis, lipolysis, and inflammatory [...] Read more.
The efficacy of α-cubebenol isolated from Schisandra chinensis has been studied in several diseases, including cecal ligation, puncture challenge-induced sepsis, and degranulation of neutrophils. To identify the novel functions of α-cubebenol on lipid metabolism, alterations on the regulation of lipogenesis, lipolysis, and inflammatory response were observed in 3T3-L1 adipocytes treated with α-cubebenol. Most lipogenic targets, including lipid accumulation, level of lipogenic transcription factors, and expression of lipogenic regulators, were suppressed in MDI (3-isobutyl-1-methylxanthine, dexamethasone, and insulin)-stimulated 3T3-L1 adipocytes treated with α-cubebenol without significant cytotoxicity. In addition, similar inhibition effects were observed in the iNOS-induced COX-2 mediated pathway and NLRP3 inflammasome pathway of MDI-stimulated 3T3-L1 cells treated with α-cubebenol. Lipolytic targets, such as cAMP concentration, expression of adenylyl cyclase and PDE4, and their downstream signaling pathway, in MDI-stimulated 3T3-L1 cells were stimulated by the α-cubebenol treatment. The levels of transcription factors and related proteins for β-oxidation were significantly higher in the MDI + α-cubebenol treated group than in the MDI + Vehicle treated group. These results show that α-cubebenol has a novel role as a lipogenesis inhibitor, lipolysis and β-oxidation stimulator, and inflammasome suppressor in MDI-stimulated 3T3-L1 adipocytes. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Eating Disorders and Obesity)
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14 pages, 2488 KiB  
Article
Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells
Biomolecules 2021, 11(11), 1567; https://doi.org/10.3390/biom11111567 - 22 Oct 2021
Cited by 10 | Viewed by 1975
Abstract
Elevated level of palmitic acid (PA), a long-chain saturated fatty acid (SFA), is lipotoxic to many different types of cells including Neuro-2a (N2a) neuroblastoma cells. CD36 is a multifunctional membrane glycoprotein that acts as a fatty acid translocase (FAT) facilitating the transport of [...] Read more.
Elevated level of palmitic acid (PA), a long-chain saturated fatty acid (SFA), is lipotoxic to many different types of cells including Neuro-2a (N2a) neuroblastoma cells. CD36 is a multifunctional membrane glycoprotein that acts as a fatty acid translocase (FAT) facilitating the transport of long-chain free fatty acids (FFAs) into cells, serves a fatty acid (FA) sensing function in areas including taste buds and the proximal gut, and acts as a scavenger receptor that binds to many ligands, including FAs, collagen, oxidized low-density lipoproteins, and anionic phospholipids. However, the involvement of CD36 in FA uptake and PA lipotoxicity in N2a cells remains unclear. In this study, we examined FA uptake in BSA- and PA-treated N2a cells and investigated the involvement of CD36 in FA uptake and PA lipotoxicity in N2a cells. Our data showed that PA treatment promoted FA uptake in N2a cells, and that treatment with sulfo-N-succinimidyl oleate (SSO), a CD36 inhibitor, significantly decreased FA uptake in BSA- and PA-treated N2a cells, and ameliorated PA-induced decrease of cell viability, decrease of diploid cells, and increase of tetraploid cells. We also found that CD36 knockdown significantly decreased FA uptake in both BSA- and PA-treated cells as compared to their corresponding wild-type controls, and dramatically attenuated PA-induced cell cycle defects in N2a cells. Our data suggest that CD36 may play a critical role in FA uptake and PA lipotoxicity in N2a cells. CD36 may therefore represent a regulatory target against pathologies caused by excess FAs. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Eating Disorders and Obesity)
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Review

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37 pages, 790 KiB  
Review
Systematic Review of Binge Eating Rodent Models for Developing Novel or Repurposing Existing Pharmacotherapies
Biomolecules 2023, 13(5), 742; https://doi.org/10.3390/biom13050742 - 25 Apr 2023
Cited by 1 | Viewed by 1499
Abstract
Recent advances in developing and screening candidate pharmacotherapies for psychiatric disorders have depended on rodent models. Eating disorders are a set of psychiatric disorders that have traditionally relied on behavioral therapies for effective long-term treatment. However, the clinical use of Lisdexamfatamine for binge [...] Read more.
Recent advances in developing and screening candidate pharmacotherapies for psychiatric disorders have depended on rodent models. Eating disorders are a set of psychiatric disorders that have traditionally relied on behavioral therapies for effective long-term treatment. However, the clinical use of Lisdexamfatamine for binge eating disorder (BED) has furthered the notion of using pharmacotherapies for treating binge eating pathologies. While there are several binge eating rodent models, there is not a consensus on how to define pharmacological effectiveness within these models. Our purpose is to provide an overview of the potential pharmacotherapies or compounds tested in established rodent models of binge eating behavior. These findings will help provide guidance for determining pharmacological effectiveness for potential novel or repurposed pharmacotherapies. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Eating Disorders and Obesity)
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15 pages, 2992 KiB  
Review
Diet Impact on Obesity beyond Calories and Trefoil Factor Family 2 (TFF2) as an Illustration: Metabolic Implications and Potential Applications
Biomolecules 2021, 11(12), 1830; https://doi.org/10.3390/biom11121830 - 04 Dec 2021
Cited by 5 | Viewed by 2325
Abstract
Obesity is a health problem with increasing impacts on public health, economy and even social life. In order to reestablish the energy balance, obesity management focuses mainly on two pillars; exercise and diet. Beyond the contribution to the caloric intake, the diet nutrients [...] Read more.
Obesity is a health problem with increasing impacts on public health, economy and even social life. In order to reestablish the energy balance, obesity management focuses mainly on two pillars; exercise and diet. Beyond the contribution to the caloric intake, the diet nutrients and composition govern a variety of properties. This includes the energy balance-independent properties and the indirect metabolic effects. Whereas the energy balance-independent properties are close to “pharmacological” effects and include effects such as antioxidant and anti-inflammatory, the indirect metabolic effects represent the contribution a diet can have on energy metabolism beyond the caloric contribution itself, which include the food intake control and metabolic changes. As an illustration, we also described the metabolic implication and hypothetical pathways of the high-fat diet-induced gene Trefoil Factor Family 2. The properties the diet has can have a variety of applications mainly in pharmacology and nutrition and further explore the “pharmacologically” active food towards potential therapeutic applications. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Eating Disorders and Obesity)
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