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Biomedicines
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Molecular Research in Obesity
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Molecular Research in Obesity

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 4519

Special Issue Editors

Dr. Zaida Abad-Jiménez

E-Mail Website
Guest Editor
Department of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), 46017 Valencia, Spain
Interests: obesity; bariatric surgery; leukocytes; oxidative stress; metabolic pathways
Dr. Teresa Vezza

E-Mail Website
Guest Editor
Servicio de Digestivo, Hospital Universitario Virgen de las Nieves, 18014 Granada, Spain
Interests: obesity; metabolic disorders; inflammation; oxidative stress; mitochondrial dysfunction

Special Issue Information

Dear Colleagues,

Obesity is a complex chronic disease of epidemic proportions, contributing to the increasing burdens of cardiovascular disease, type 2 diabetes, hyperlipidemia, and premature death worldwide. Although the rapid increase in obesity has been driven by environmental changes, genetic factors are also critical players in determining individual predisposition to this condition.

Obesity has been linked to adverse alterations in adipose tissue, specifically white and brown adipose tissue, that predisposes subjects to metabolic dysregulation, chronic low-grade inflammation, and dysfunction in energy storage and expenditure. These adverse alterations include the activation and/or inhibition of relevant molecular pathways regulating appetite, metabolism, energy balance, adipocyte differentiation, and thermogenesis. Although mechanisms beyond obesity and its related comorbidities have been extensively investigated, some of them have yet to be fully elucidated.

This Special Issue aims to summarize the current knowledge and advances in this field, showcasing the novel molecular mechanisms underlying obesity; to prevent the individual risk of developing obesity; and to identify novel approaches in the management of this condition.

Original research articles and reviews include (but are not limited to): elucidating the molecular underpinnings of obesity, identifying genetic factors, unraveling metabolic pathways, and exploring the functions of adipose tissue.

Dr. Zaida Abad-Jiménez
Dr. Teresa Vezza
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. Biomedicines 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 2600 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
  • genetics
  • molecular pathways
  • adipose tissue
  • metabolism
  • leukocytes
  • prevention
  • new targets for treatment
  • translational studies

Published Papers (4 papers)

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Research

Jump to: Review

17 pages, 3245 KiB  
Article
Neurosecretory Protein GM–Expressing Neurons Participate in Lipid Storage and Inflammation in Newly Developed Cre Driver Male Mice
by Yuki Narimatsu, Masaki Kato, Eiko Iwakoshi-Ukena, Shogo Moriwaki, Ayano Ogasawara, Megumi Furumitsu and Kazuyoshi Ukena
Biomedicines 2023, 11(12), 3230; https://doi.org/10.3390/biomedicines11123230 - 06 Dec 2023
Viewed by 888
Abstract
Obesity induces inflammation in the hypothalamus and adipose tissue, resulting in metabolic disorders. A novel hypothalamic neuropeptide, neurosecretory protein GM (NPGM), was previously identified in the hypothalamus of vertebrates. While NPGM plays an important role in lipid metabolism in chicks, its metabolic regulatory [...] Read more.
Obesity induces inflammation in the hypothalamus and adipose tissue, resulting in metabolic disorders. A novel hypothalamic neuropeptide, neurosecretory protein GM (NPGM), was previously identified in the hypothalamus of vertebrates. While NPGM plays an important role in lipid metabolism in chicks, its metabolic regulatory effects in mammals remain unclear. In this study, a novel Cre driver line, NPGM-Cre, was generated for cell-specific manipulation. Cre-dependent overexpression of Npgm led to fat accumulation without increased food consumption in male NPGM-Cre mice. Chemogenetic activation of NPGM neurons in the hypothalamus acutely promoted feeding behavior and chronically resulted in a transient increase in body mass gain. Furthermore, the ablated NPGM neurons exhibited a tendency to be glucose intolerant, with infiltration of proinflammatory macrophages into the adipose tissue. These results suggest that NPGM neurons may regulate lipid storage and inflammatory responses, thereby maintaining glucose homeostasis. Full article
(This article belongs to the Special Issue Molecular Research in Obesity)
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15 pages, 1555 KiB  
Article
Effect of Bariatric Surgery on Plasma Cell-Free Mitochondrial DNA, Insulin Sensitivity and Metabolic Changes in Obese Patients
by Larysa V. Yuzefovych, Viktor M. Pastukh, Madhuri S. Mulekar, Kate Ledbetter, William O. Richards and Lyudmila I. Rachek
Biomedicines 2023, 11(9), 2514; https://doi.org/10.3390/biomedicines11092514 - 12 Sep 2023
Viewed by 816
Abstract
While improvement of mitochondrial function after bariatric surgery has been demonstrated, there is limited evidence about the effects of bariatric surgery on circulatory cell-free (cf) mitochondrial DNA (mtDNA) and intracellular mtDNA abundance. Plasma and peripheral blood mononuclear (PBM) cells were isolated from healthy [...] Read more.
While improvement of mitochondrial function after bariatric surgery has been demonstrated, there is limited evidence about the effects of bariatric surgery on circulatory cell-free (cf) mitochondrial DNA (mtDNA) and intracellular mtDNA abundance. Plasma and peripheral blood mononuclear (PBM) cells were isolated from healthy controls (HC) and bariatric surgery patients before surgery and 2 weeks, 3 months, and 6 months after surgery. At baseline, the plasma level of short cf-mtDNA (ND6, ~100 bp) fragments was significantly higher in obese patients compared to HC. But there was no significant variation in mean ND6 values post-surgery. A significant positive correlation was observed between preop plasma ND6 levels and HgbA1c, ND6 and HOMA-IR 2 weeks post-surgery, and mtDNA content 6 months post-surgery. Interestingly, plasma from both HC and obese groups at all time points post-surgery contains long (~8 kb) cf-mtDNA fragments, suggesting the presence of near-intact and/or whole mitochondrial genomes. No significant variation was observed in mtDNA content post-surgery compared to baseline data in both PBM and skeletal muscle samples. Overall, bariatric surgery improved insulin sensitivity and other metabolic parameters without significant changes in plasma short cf-mtDNA levels or cellular mtDNA content. Our study provides novel insights about possible molecular mechanisms underlying the metabolic effects of bariatric surgery and suggests the development of new generalized approaches to characterize cf-mtDNA. Full article
(This article belongs to the Special Issue Molecular Research in Obesity)
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13 pages, 1800 KiB  
Article
Circulating and Exosomal microRNA-33 in Childhood Obesity
by Manuela Cabiati, Letizia Guiducci, Emioli Randazzo, Valentina Casieri, Giovanni Federico and Silvia Del Ry
Biomedicines 2023, 11(8), 2295; https://doi.org/10.3390/biomedicines11082295 - 18 Aug 2023
Viewed by 796
Abstract
Background: MicroRNA-33 may control a wide range of different metabolic functions. Methods: This study aims to assess the miR-33a circulating profile in normal-weight (N = 20) and obese (O = 30) adolescents and to correlate its expression levels to their metabolic parameters. In [...] Read more.
Background: MicroRNA-33 may control a wide range of different metabolic functions. Methods: This study aims to assess the miR-33a circulating profile in normal-weight (N = 20) and obese (O = 30) adolescents and to correlate its expression levels to their metabolic parameters. In a subset of subjects, we compared circulating miR-33a with exosomal miR-33a. Results: Metabolic parameters were altered in O, with initial hyperinsulinemia. Circulating miR-33a was significantly higher in O than in N (p = 0.0002). Significant correlations between miR-33a and auxological and metabolic indices (Insulin p = 0.01; Cholesterol p = 0.01; LDL p = 0.01; HbA1c p = 0.01) were found. Splitting our population (O + N) into two groups, according to the median value of mRNA expression miR-33a levels (0.701), irrespective of the presence or absence of obesity, we observed that those having a higher expression of miR-33a were more frequently obese (87.5% vs. 12.5%; p < 0.0001) and had significantly increased values of auxological and metabolic parameters. Exosomes extracted from plasma of N and O carried miR-33a, and its expression was lower in O (p = 0.026). No correlations with metabolic parameters were observed. Conclusion: While exosome miR-33a does not provide any advantage, circulating miR-33a can provide important indications in an initial phase of metabolic dysfunction, stratifying obese adolescents at higher cardiometabolic risk. Full article
(This article belongs to the Special Issue Molecular Research in Obesity)
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Review

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22 pages, 1369 KiB  
Review
Methylglyoxal and Advanced Glycation End Products (AGEs): Targets for the Prevention and Treatment of Diabetes-Associated Bladder Dysfunction?
by Akila Lara Oliveira, Mariana Gonçalves de Oliveira, Fabíola Zakia Mónica and Edson Antunes
Biomedicines 2024, 12(5), 939; https://doi.org/10.3390/biomedicines12050939 - 23 Apr 2024
Viewed by 435
Abstract
Methylglyoxal (MGO) is a highly reactive α-dicarbonyl compound formed endogenously from 3-carbon glycolytic intermediates. Methylglyoxal accumulated in plasma and urine of hyperglycemic and diabetic individuals acts as a potent peptide glycation molecule, giving rise to advanced glycation end products (AGEs) like arginine-derived hydroimidazolone [...] Read more.
Methylglyoxal (MGO) is a highly reactive α-dicarbonyl compound formed endogenously from 3-carbon glycolytic intermediates. Methylglyoxal accumulated in plasma and urine of hyperglycemic and diabetic individuals acts as a potent peptide glycation molecule, giving rise to advanced glycation end products (AGEs) like arginine-derived hydroimidazolone (MG-H1) and carboxyethyl-lysine (CEL). Methylglyoxal-derived AGEs exert their effects mostly via activation of RAGE, a cell surface receptor that initiates multiple intracellular signaling pathways, favoring a pro-oxidant environment through NADPH oxidase activation and generation of high levels of reactive oxygen species (ROS). Diabetic bladder dysfunction is a bothersome urological complication in patients with poorly controlled diabetes mellitus and may comprise overactive bladder, urge incontinence, poor emptying, dribbling, incomplete emptying of the bladder, and urinary retention. Preclinical models of type 1 and type 2 diabetes have further confirmed the relationship between diabetes and voiding dysfunction. Interestingly, healthy mice supplemented with MGO for prolonged periods exhibit in vivo and in vitro bladder dysfunction, which is accompanied by increased AGE formation and RAGE expression, as well as by ROS overproduction in bladder tissues. Drugs reported to scavenge MGO and to inactivate AGEs like metformin, polyphenols, and alagebrium (ALT-711) have shown favorable outcomes on bladder dysfunction in diabetic obese leptin-deficient and MGO-exposed mice. Therefore, MGO, AGEs, and RAGE levels may be critically involved in the pathogenesis of bladder dysfunction in diabetic individuals. However, there are no clinical trials designed to test drugs that selectively inhibit the MGO–AGEs–RAGE signaling, aiming to reduce the manifestations of diabetes-associated bladder dysfunction. This review summarizes the current literature on the role of MGO–AGEs–RAGE–ROS axis in diabetes-associated bladder dysfunction. Drugs that directly inactivate MGO and ameliorate bladder dysfunction are also reviewed here. Full article
(This article belongs to the Special Issue Molecular Research in Obesity)
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